Neurobiology Flashcards

Question

Each of the following occurs in phototransduction except A. Activated rhodopsin activates a G protein. B. Activation of cyclic guanosine monophosphate (cGMP) phosphodiesterase increases hydrolysis of cGMP to 59-GMP. C. Current through a cGMP-activated sodium channel decreases. D. Rhodopsin is activated when light converts bound 11-cis-retinal to alltrans-retinal. E. The decreased concentration of cGMP results in depolarization of the plasma membrane.

Answer 1

A. Activated rhodopsin activates a G protein. B. Activation of cyclic guanosine monophosphate (cGMP) phosphodiesterase increases hydrolysis of cGMP to 59-GMP. C. Current through a cGMP-activated sodium channel decreases. D. Rhodopsin is activated when light converts bound 11-cis-retinal to alltrans-retinal. **E. The decreased concentration of cGMP results in depolarization of the plasma membrane.** ## Footnote In p h otot ran sd u ct ion , a p h oton of ligh t lead s to t h e isomerization of 11-cisretinal to an all-trans form , activating rhodopsin (D). Ac t ivat e d rh o d o p s i n then stimulates a G-protein-coupled receptor, transducin (A), activating a cyclic GMP-speci c phosphodiesterase (PDE [B]). Th e d ecreased cGMP level (caused by increased cGMP PDE) leads to a decreased Na conductance by cGMP-gated ion channels (C) lead in g to hyp er p olar izat ion of t h e m em bran e. In su m m ar y, light leads to hyperpolarization of the cell membrane via reduced levels of cGMP (E is false). 5

Answer 2

**A. Each G protein is regulated by only one type of receptor.** B. Each G protein may regulate multiple e ectors. C. The a subun it bin ds guan osin e t riph osph ate (GTP). D. The b an d g su bun its h elp an ch or th e a subu n it to th e plasm a m em bran e. E. The b and g subunits modulate guanosine diphosphate (GDP)/GTP exchange. ## Footnote G p rotein s bin d to t h e cytop lasm ic face of a given receptor; each G protein may be regulated by separate receptors (A is false). Agon ist s p rom ote th e binding of GTP to the a subunit (C), w h ich can t h en act ivate a variety of e ector proteins (B). Th e G p rotein rem ain s act ive u n t il GTP is hyd rolyzed to GDP. The b an d γ su bu n it s h elp to anchor the G protein to the membrane (D), participate in modulation of GDP/GTP exchange (E), an d con fer localization via myristolization. 2,5

Answer 3

A. Calcium B. 1,2-Diacylglycerol (DAG) **C. Cyclic adenosine monophosphate (cAMP)** D. Cyclic guanine monophosphate (cGMP) E. Inositol-1,4,5-trisphosphate (IP3) F. B an d E ## Footnote Cyt o s o lic calcium (A) levels are regu lated by several di eren t factors, an d calcium (A) m ay e xe r t it s in u e n ce via m u lt ip le m e ch a n ism s—ca lciu m is t h e o n ly choice listed, however, that binds to calm odulin. Gq activates phospholipase C w h ich h yd r o lyz e s p h o s p h a t id ylin o s it o l- 4 ,5 - b is p h o s p h a t e t o inositol-1,4,5trisphosphate (IP3 [E]) and diacylglycerol (DAG [B]). IP3 (E) binds to receptors on the endoplasmic reticulum that cause a transient increase in cytosolic calcium concentrations. DAG (B) binds protein kinase C (PKC), lowering PKC’s requirement for activation by calcium. Cy c l i c AMP ( c AMP [ C] ) is generated by adenylyl cyclase, stimulated by Gs , an d in h ibited by Gi . D1 receptors are an example of a receptor that uses cAMP (C) as a second m essenger. Nitric oxide generates cyclic GMP (cGMP [D]) via activation of soluble guanylyl cyclase. Ph otorecept ion ut ilizes cGMP (D) a s a s e co n d m e ss e n ge r. Re ca ll t h a t ligh t le a d s to hyperpolarization of the cell membrane via reduced levels of cGMP (D). 5

Answer 4

A. Calcium B. 1,2-Diacylglycerol (DAG) C. Cyclic adenosine monophosphate (cAMP) **D. Cyclic guanine monophosphate (cGMP)** E. Inositol-1,4,5-trisphosphate (IP3) F. B an d E ## Footnote Cyt o s o lic calcium (A) levels are regu lated by several di eren t factors, an d calcium (A) m ay e xe r t it s in u e n ce via m u lt ip le m e ch a n ism s—ca lciu m is t h e o n ly choice listed, however, that binds to calm odulin. Gq activates phospholipase C w h ich h yd r o lyz e s p h o s p h a t id ylin o s it o l- 4 ,5 - b is p h o s p h a t e t o inositol-1,4,5trisphosphate (IP3 [E]) and diacylglycerol (DAG [B]). IP3 (E) binds to receptors on the endoplasmic reticulum that cause a transient increase in cytosolic calcium concentrations. DAG (B) binds protein kinase C (PKC), lowering PKC’s requirement for activation by calcium. Cy c l i c AMP ( c AMP [ C] ) is generated by adenylyl cyclase, stimulated by Gs , an d in h ibited by Gi . D1 receptors are an example of a receptor that uses cAMP (C) as a second m essenger. Nitric oxide generates cyclic GMP (cGMP [D]) via activation of soluble guanylyl cyclase. Ph otorecept ion ut ilizes cGMP (D) a s a s e co n d m e ss e n ge r. Re ca ll t h a t ligh t le a d s to hyperpolarization of the cell membrane via reduced levels of cGMP (D). 5

Answer 5

A. Calcium B. 1,2-Diacylglycerol (DAG) C. Cyclic adenosine monophosphate (cAMP) D. Cyclic guanine monophosphate (cGMP) E. Inositol-1,4,5-trisphosphate (IP3) **F. B an d E** ## Footnote Cyt o s o lic calcium (A) levels are regu lated by several di eren t factors, an d calcium (A) m ay e xe r t it s in u e n ce via m u lt ip le m e ch a n ism s—ca lciu m is t h e o n ly choice listed, however, that binds to calm odulin. Gq activates phospholipase C w h ich h yd r o lyz e s p h o s p h a t id ylin o s it o l- 4 ,5 - b is p h o s p h a t e t o inositol-1,4,5trisphosphate (IP3 [E]) and diacylglycerol (DAG [B]). IP3 (E) binds to receptors on the endoplasmic reticulum that cause a transient increase in cytosolic calcium concentrations. DAG (B) binds protein kinase C (PKC), lowering PKC’s requirement for activation by calcium. Cy c l i c AMP ( c AMP [ C] ) is generated by adenylyl cyclase, stimulated by Gs , an d in h ibited by Gi . D1 receptors are an example of a receptor that uses cAMP (C) as a second m essenger. Nitric oxide generates cyclic GMP (cGMP [D]) via activation of soluble guanylyl cyclase. Ph otorecept ion ut ilizes cGMP (D) a s a s e co n d m e ss e n ge r. Re ca ll t h a t ligh t le a d s to hyperpolarization of the cell membrane via reduced levels of cGMP (D). 5

Answer 6

A. Calcium **B. 1,2-Diacylglycerol (DAG)** C. Cyclic adenosine monophosphate (cAMP) D. Cyclic guanine monophosphate (cGMP) E. Inositol-1,4,5-trisphosphate (IP3) F. B an d E ## Footnote Cyt o s o lic calcium (A) levels are regu lated by several di eren t factors, an d calcium (A) m ay e xe r t it s in u e n ce via m u lt ip le m e ch a n ism s—ca lciu m is t h e o n ly choice listed, however, that binds to calm odulin. Gq activates phospholipase C w h ich h yd r o lyz e s p h o s p h a t id ylin o s it o l- 4 ,5 - b is p h o s p h a t e t o inositol-1,4,5trisphosphate (IP3 [E]) and diacylglycerol (DAG [B]). IP3 (E) binds to receptors on the endoplasmic reticulum that cause a transient increase in cytosolic calcium concentrations. DAG (B) binds protein kinase C (PKC), lowering PKC’s requirement for activation by calcium. Cy c l i c AMP ( c AMP [ C] ) is generated by adenylyl cyclase, stimulated by Gs , an d in h ibited by Gi . D1 receptors are an example of a receptor that uses cAMP (C) as a second m essenger. Nitric oxide generates cyclic GMP (cGMP [D]) via activation of soluble guanylyl cyclase. Ph otorecept ion ut ilizes cGMP (D) a s a s e co n d m e ss e n ge r. Re ca ll t h a t ligh t le a d s to hyperpolarization of the cell membrane via reduced levels of cGMP (D). 5

Answer 7

**A. Calcium** B. 1,2-Diacylglycerol (DAG) C. Cyclic adenosine monophosphate (cAMP) D. Cyclic guanine monophosphate (cGMP) E. Inositol-1,4,5-trisphosphate (IP3) F. B an d E ## Footnote Cyt o s o lic calcium (A) levels are regu lated by several di eren t factors, an d calcium (A) m ay e xe r t it s in u e n ce via m u lt ip le m e ch a n ism s—ca lciu m is t h e o n ly choice listed, however, that binds to calm odulin. Gq activates phospholipase C w h ich h yd r o lyz e s p h o s p h a t id ylin o s it o l- 4 ,5 - b is p h o s p h a t e t o inositol-1,4,5trisphosphate (IP3 [E]) and diacylglycerol (DAG [B]). IP3 (E) binds to receptors on the endoplasmic reticulum that cause a transient increase in cytosolic calcium concentrations. DAG (B) binds protein kinase C (PKC), lowering PKC’s requirement for activation by calcium. Cy c l i c AMP ( c AMP [ C] ) is generated by adenylyl cyclase, stimulated by Gs , an d in h ibited by Gi . D1 receptors are an example of a receptor that uses cAMP (C) as a second m essenger. Nitric oxide generates cyclic GMP (cGMP [D]) via activation of soluble guanylyl cyclase. Ph otorecept ion ut ilizes cGMP (D) a s a s e co n d m e ss e n ge r. Re ca ll t h a t ligh t le a d s to hyperpolarization of the cell membrane via reduced levels of cGMP (D). 5

Answer 8

A. Calcium B. 1,2-Diacylglycerol (DAG) C. Cyclic adenosine monophosphate (cAMP) **D. Cyclic guanine monophosphate (cGMP)** E. Inositol-1,4,5-trisphosphate (IP3) F. B an d E ## Footnote Cyt o s o lic calcium (A) levels are regu lated by several di eren t factors, an d calcium (A) m ay e xe r t it s in u e n ce via m u lt ip le m e ch a n ism s—ca lciu m is t h e o n ly choice listed, however, that binds to calm odulin. Gq activates phospholipase C w h ich h yd r o lyz e s p h o s p h a t id ylin o s it o l- 4 ,5 - b is p h o s p h a t e t o inositol-1,4,5trisphosphate (IP3 [E]) and diacylglycerol (DAG [B]). IP3 (E) binds to receptors on the endoplasmic reticulum that cause a transient increase in cytosolic calcium concentrations. DAG (B) binds protein kinase C (PKC), lowering PKC’s requirement for activation by calcium. Cy c l i c AMP ( c AMP [ C] ) is generated by adenylyl cyclase, stimulated by Gs , an d in h ibited by Gi . D1 receptors are an example of a receptor that uses cAMP (C) as a second m essenger. Nitric oxide generates cyclic GMP (cGMP [D]) via activation of soluble guanylyl cyclase. Ph otorecept ion ut ilizes cGMP (D) a s a s e co n d m e ss e n ge r. Re ca ll t h a t ligh t le a d s to hyperpolarization of the cell membrane via reduced levels of cGMP (D). 5

Answer 9

A. Calcium B. 1,2-Diacylglycerol (DAG) C. Cyclic adenosine monophosphate (cAMP) D. Cyclic guanine monophosphate (cGMP) **E. Inositol-1,4,5-trisphosphate (IP3)** F. B an d E ## Footnote Cyt o s o lic calcium (A) levels are regu lated by several di eren t factors, an d calcium (A) m ay e xe r t it s in u e n ce via m u lt ip le m e ch a n ism s—ca lciu m is t h e o n ly choice listed, however, that binds to calm odulin. Gq activates phospholipase C w h ich h yd r o lyz e s p h o s p h a t id ylin o s it o l- 4 ,5 - b is p h o s p h a t e t o inositol-1,4,5trisphosphate (IP3 [E]) and diacylglycerol (DAG [B]). IP3 (E) binds to receptors on the endoplasmic reticulum that cause a transient increase in cytosolic calcium concentrations. DAG (B) binds protein kinase C (PKC), lowering PKC’s requirement for activation by calcium. Cy c l i c AMP ( c AMP [ C] ) is generated by adenylyl cyclase, stimulated by Gs , an d in h ibited by Gi . D1 receptors are an example of a receptor that uses cAMP (C) as a second m essenger. Nitric oxide generates cyclic GMP (cGMP [D]) via activation of soluble guanylyl cyclase. Ph otorecept ion ut ilizes cGMP (D) a s a s e co n d m e ss e n ge r. Re ca ll t h a t ligh t le a d s to hyperpolarization of the cell membrane via reduced levels of cGMP (D). 5

Answer 10

A. Contributes to the resting potential of the cell B. Hyperpolarizes the membrane C. Is electrogenic D. Transports three Na 1 ion s out for t w o K 1 ion s in **E. Utilizes two molecules of adenosine triphosphate (ATP) for every three Na 1 ions transported** ## Footnote Th e sod iu m p ot a ssiu m ATPase con t r ib u t es t o t h e resting potential of the cell (A); hyperpolarizing the membrane (B) by p u m p in g three Na 1 ions into the cell for every two K 1 ions it transports out of the cell (D). Th is act ion gen erates both a chemical and an electrical gradient (C) across t h e cell m e m bran e. Th e Na 1 /K 1 pump uses one molecule of adenosine triphosphate (ATP) for every three Na 1 ions transported (E is false). 5

Answer 11

A. A sudden increase in conductance of Na results in depolarization. **B. Chloride permeability increases during depolarization.** C. During hyperpolarization, the conductance of Na is lower than normal, and the conductance of K is higher than normal. D. The decrease in Na permeability, occurring as the action potential reaches a peak, results from inactivation of Na channels. E. The presence of voltage-dependent K channels is to allow faster repolarization. ## Footnote An a c t io n p o t e n t ia l co n s is t s o f t w o p h a s e s , t h e r s t o f w h ich is d u e t o a n increased perm eability to Na caused by the opening of voltage-gated Na channels (A). Th u s th ere is rap id d ep olarizat ion of th e cell d u e to sod iu m in ux. The second phase is due to fast activation of Na channels (D) and delayed opening of K channels that allow K to leave the cell and terminate depolarization (C, E). Ch lorid e p erm eabilit y d oes n ot ch ange d u ring t h e action potential (B is false). 5

Answer 12

A. High transmembrane resistance, low internal resistance, and high membrane capacitance **B. High transmembrane resistance, low internal resistance, and low membrane capacitance** C. Low transmembrane resistance, high internal resistance, and high membrane capacitance D. Low transmembrane resistance, low internal resistance, and high membrane capacitance E. Low transmembrane resistance, low internal resistance, and low membrane capacitance ## Footnote Th e velocit y of an a ct ion p ot e n t ial in crea ses w it h high transmembrane resistance, low internal resistance, and low membrane capacitance (B). Th e conduction velocity is dependent on the diam eter of the axon and myelination status. Increased axonal diameter leads to lower internal resistance and higher conduction velocities. Myelination leads to increased velocities via increased transm em brane resistance and decreased m em brane capacitance, and therefore higher conduction velocities. 7

Answer 13

A. It has no e ect on transmembrane resistance but increases membrane c a p a c i t a n c e . B. It decreases both transmembrane resistance and membrane capacitance. C. It decreases transmembrane resistance and increases membrane c a p a c i t a n c e . **D. It increases transmembrane resistance and decreases membrane c a p a c i t a n c e . ** E. It increases both transmembrane resistance and membrane capacitance. ## Footnote Myelination increases transm em brane resistance and decreases m em brane capacitance, leading to increased conduction velocities. 6

Answer 14

**A. End-plate potential** B. Miniature end-plate potential C. Both D. Neither ## Footnote En d - p l at e p o t e n t ia l (A) refers to the depolarizing process that occurs at the neuromuscular junction, triggering a muscle action potential, and therefore leading to m uscle contraction. Miniature end-plate potentials (B) result from random release of quanta of acet ylcholine causing m inor regional m em brane depolarizations (excitatory end-plate potentials) but do not reach the threshold necessary to produce an action potential. Action potentials are an all-or-nothing phenomenon (D). 5

Answer 15

A. End-plate potential **B. Miniature end-plate potential** C. Both D. Neither ## Footnote En d - p l at e p o t e n t ia l (A) refers to the depolarizing process that occurs at the neuromuscular junction, triggering a muscle action potential, and therefore leading to m uscle contraction. Miniature end-plate potentials (B) result from random release of quanta of acet ylcholine causing m inor regional m em brane depolarizations (excitatory end-plate potentials) but do not reach the threshold necessary to produce an action potential. Action potentials are an all-or-nothing phenomenon (D). 5

Answer 16

A. End-plate potential B. Miniature end-plate potential C. Both **D. Neither** ## Footnote En d - p l at e p o t e n t ia l (A) refers to the depolarizing process that occurs at the neuromuscular junction, triggering a muscle action potential, and therefore leading to m uscle contraction. Miniature end-plate potentials (B) result from random release of quanta of acet ylcholine causing m inor regional m em brane depolarizations (excitatory end-plate potentials) but do not reach the threshold necessary to produce an action potential. Action potentials are an all-or-nothing phenomenon (D). 5

Answer 17

A. Cl 2 only **B. Cl 2 or K 1** C. Na 1 on ly D. Na 1 or Cl 2 E. Na 1 or K 1 ## Footnote Lo c a l i z e d d e p o l a r i z a t i o n s o f t h e c e l l m e m b r a n e a r e u s u a l ly d u e t o i n c r e a s e d Na 1 permeability (C) and are called excitatory postsynaptic potentials (EPSPs). The sum m ation of m ultiple EPSPs can cause an action potential to occur if the depolarization reaches threshold. This e ect can be blocked by inhibitory postsynaptic potentials (IPSPs) that represent regional hyperpolarization m ediated by increased perm eability to Cl 2 or K 1 ions (B). 5

Answer 18

**A. Dynamin does not use ATP.** B. Dynein is the motor for anterograde fast axonal transport. C. Fast axonal transport occurs primarily along neuro laments. D. Kinesin is the motor for retrograde fast axonal transport. E. Slow axonal transport occurs at 200 to 400 mm/day. ## Footnote Dynam in uses GTP a s a n e n e r g y s o u rc e (A) . Dyn ein is t h e m otor p rotein for retrograde fast axonal transport (B and E are false). Slow a xon al t ran sp or t occurs at several millimeters per day (E is false); fast axonal transport occurs at 200 to 400 mm/day and utilizes microtubules (C is false). 2,6

Answer 19

A. Golgi tendon organ B. Muscle spindle **C. Both** D. Neither ## Footnote Bo t h Go l g i t e n d o n o rg a n s (A) and muscle spindles (B) are proprioceptive receptors that are activated by passive stretch and are innervated by group I (large myelinated) bers. Go l g i t e n d o n o rg a n s (A) are ar ran ge d in se r ies w it h the muscle in the tendon and are activated maximally by muscle contraction. Muscle spindles (B) are arranged in parallel w ith the m uscle bers and consist of a dynam ic nuclear bag, static nuclear bag, and nuclear chain bers. Muscle spindles are sensitive to muscle stretch and length. Motor innervation to the muscle spindle via gamma motor neurons allows for the length of the muscle spindle to change its sensitivity to length and velocity of length change. 6,8

Answer 20

**A. Golgi tendon organ** B. Muscle spindle C. Both D. Neither ## Footnote Bo t h Go l g i t e n d o n o rg a n s (A) and muscle spindles (B) are proprioceptive receptors that are activated by passive stretch and are innervated by group I (large myelinated) bers. Go l g i t e n d o n o rg a n s (A) are ar ran ge d in se r ies w it h the muscle in the tendon and are activated maximally by muscle contraction. Muscle spindles (B) are arranged in parallel w ith the m uscle bers and consist of a dynam ic nuclear bag, static nuclear bag, and nuclear chain bers. Muscle spindles are sensitive to muscle stretch and length. Motor innervation to the muscle spindle via gamma motor neurons allows for the length of the muscle spindle to change its sensitivity to length and velocity of length change. 6,8

Answer 21

**A. Golgi tendon organ** B. Muscle spindle C. Both D. Neither ## Footnote Bo t h Go l g i t e n d o n o rg a n s (A) and muscle spindles (B) are proprioceptive receptors that are activated by passive stretch and are innervated by group I (large myelinated) bers. Go l g i t e n d o n o rg a n s (A) are ar ran ge d in se r ies w it h the muscle in the tendon and are activated maximally by muscle contraction. Muscle spindles (B) are arranged in parallel w ith the m uscle bers and consist of a dynam ic nuclear bag, static nuclear bag, and nuclear chain bers. Muscle spindles are sensitive to muscle stretch and length. Motor innervation to the muscle spindle via gamma motor neurons allows for the length of the muscle spindle to change its sensitivity to length and velocity of length change. 6,8

Answer 22

A. Golgi tendon organ **B. Muscle spindle** C. Both D. Neither ## Footnote Bo t h Go l g i t e n d o n o rg a n s (A) and muscle spindles (B) are proprioceptive receptors that are activated by passive stretch and are innervated by group I (large myelinated) bers. Go l g i t e n d o n o rg a n s (A) are ar ran ge d in se r ies w it h the muscle in the tendon and are activated maximally by muscle contraction. Muscle spindles (B) are arranged in parallel w ith the m uscle bers and consist of a dynam ic nuclear bag, static nuclear bag, and nuclear chain bers. Muscle spindles are sensitive to muscle stretch and length. Motor innervation to the muscle spindle via gamma motor neurons allows for the length of the muscle spindle to change its sensitivity to length and velocity of length change. 6,8

Answer 23

A. Golgi tendon organ **B. Muscle spindle** C. Both D. Neither ## Footnote Bo t h Go l g i t e n d o n o rg a n s (A) and muscle spindles (B) are proprioceptive receptors that are activated by passive stretch and are innervated by group I (large myelinated) bers. Go l g i t e n d o n o rg a n s (A) are ar ran ge d in se r ies w it h the muscle in the tendon and are activated maximally by muscle contraction. Muscle spindles (B) are arranged in parallel w ith the m uscle bers and consist of a dynam ic nuclear bag, static nuclear bag, and nuclear chain bers. Muscle spindles are sensitive to muscle stretch and length. Motor innervation to the muscle spindle via gamma motor neurons allows for the length of the muscle spindle to change its sensitivity to length and velocity of length change. 6,8

Answer 24

A. Golgi tendon organ **B. Muscle spindle** C. Both D. Neither ## Footnote Bo t h Go l g i t e n d o n o rg a n s (A) and muscle spindles (B) are proprioceptive receptors that are activated by passive stretch and are innervated by group I (large myelinated) bers. Go l g i t e n d o n o rg a n s (A) are ar ran ge d in se r ies w it h the muscle in the tendon and are activated maximally by muscle contraction. Muscle spindles (B) are arranged in parallel w ith the m uscle bers and consist of a dynam ic nuclear bag, static nuclear bag, and nuclear chain bers. Muscle spindles are sensitive to muscle stretch and length. Motor innervation to the muscle spindle via gamma motor neurons allows for the length of the muscle spindle to change its sensitivity to length and velocity of length change. 6,8

Answer 25

A. Golgi tendon organ B. Muscle spindle **C. Both** D. Neither ## Footnote Bo t h Go l g i t e n d o n o rg a n s (A) and muscle spindles (B) are proprioceptive receptors that are activated by passive stretch and are innervated by group I (large myelinated) bers. Go l g i t e n d o n o rg a n s (A) are ar ran ge d in se r ies w it h the muscle in the tendon and are activated maximally by muscle contraction. Muscle spindles (B) are arranged in parallel w ith the m uscle bers and consist of a dynam ic nuclear bag, static nuclear bag, and nuclear chain bers. Muscle spindles are sensitive to muscle stretch and length. Motor innervation to the muscle spindle via gamma motor neurons allows for the length of the muscle spindle to change its sensitivity to length and velocity of length change. 6,8

Answer 26

A. Golgi tendon organ **B. Muscle spindle** C. Both D. Neither ## Footnote Bo t h Go l g i t e n d o n o rg a n s (A) and muscle spindles (B) are proprioceptive receptors that are activated by passive stretch and are innervated by group I (large myelinated) bers. Go l g i t e n d o n o rg a n s (A) are ar ran ge d in se r ies w it h the muscle in the tendon and are activated maximally by muscle contraction. Muscle spindles (B) are arranged in parallel w ith the m uscle bers and consist of a dynam ic nuclear bag, static nuclear bag, and nuclear chain bers. Muscle spindles are sensitive to muscle stretch and length. Motor innervation to the muscle spindle via gamma motor neurons allows for the length of the muscle spindle to change its sensitivity to length and velocity of length change. 6,8

Answer 27

A. Golgi tendon organ B. Muscle spindle C. Both **D. Neither** ## Footnote Bo t h Go l g i t e n d o n o rg a n s (A) and muscle spindles (B) are proprioceptive receptors that are activated by passive stretch and are innervated by group I (large myelinated) bers. Go l g i t e n d o n o rg a n s (A) are ar ran ge d in se r ies w it h the muscle in the tendon and are activated maximally by muscle contraction. Muscle spindles (B) are arranged in parallel w ith the m uscle bers and consist of a dynam ic nuclear bag, static nuclear bag, and nuclear chain bers. Muscle spindles are sensitive to muscle stretch and length. Motor innervation to the muscle spindle via gamma motor neurons allows for the length of the muscle spindle to change its sensitivity to length and velocity of length change. 6,8

Answer 28

A. Golgi tendon organ **B. Muscle spindle** C. Both D. Neither ## Footnote Bo t h Go l g i t e n d o n o rg a n s (A) and muscle spindles (B) are proprioceptive receptors that are activated by passive stretch and are innervated by group I (large myelinated) bers. Go l g i t e n d o n o rg a n s (A) are ar ran ge d in se r ies w it h the muscle in the tendon and are activated maximally by muscle contraction. Muscle spindles (B) are arranged in parallel w ith the m uscle bers and consist of a dynam ic nuclear bag, static nuclear bag, and nuclear chain bers. Muscle spindles are sensitive to muscle stretch and length. Motor innervation to the muscle spindle via gamma motor neurons allows for the length of the muscle spindle to change its sensitivity to length and velocity of length change. 6,8

Answer 29

A. It results from tonic activity in the vestibulospinal and pontine reticulospinal neurons. B. It is reduced by cutting dorsal roots. **C. It is reduced by destruction of the anterior lobe of the cerebellum.** D. It occurs with transection between the colliculi. E. There is increased gamma motor neuron activity. ## Footnote Decerebrate rigidit y, or exten sor post uring, result s from ton ic act ivit y of th e lateral vestibular and pontine reticular nuclei (A) promoting unopposed extensor tone of the upper and lower extremities, and may be induced by transection between the colliculi (D). Decerebrate r igid it y is associated with increased gamma motor neuron activity (E) and may be reduced by sectioning of the dorsal roots (B). Dest r u ct ion of t h e an ter ior lobe of t h e cerebellum releases the cells of origin of the lateral vestibular tract from inhibition by Purkinje’s cells, thereby facilitating extensor motor neurons (C is false). 3,8

Answer 30

A. Clasp-knife response B. Flexion reflex **C. F response** D. H response E. M response F. Stretch reflex ## Footnote Th e H re ex (Ho m an’s [D]) is the electrical equivalent of the tendon re ex circuit and represents the activation of a m uscle contraction w ith subm aximal stimulation insu cient to illicit a direct motor response—the response is m ediated by the activation of m uscle spindles and involves both the dorsal and ventral horns. The H re ex (D) is particularly useful in the diagnosis of S1 rad icu lop at hy. Th e F w ave (C) is evoked by supramaximal stimulus of a mixed motor-sensory nerve and consists of a small muscle action potential recorded after the direct motor response. The F w ave resu lt s from an t id rom ic impulses traveling up the m otor nerve to the anterior horn causing an orthodromic response recorded in distal muscle. A normal F w ave and absent H re ex occur in diseases of sensory nerves and roots. The M w ave (E) is the direct motor response caused by stimulation of a motor nerve. A clasp-knife response consists of the following: if muscles are briskly stretched, the limb moves freely for a short distance followed by rapid resistance—with increasing passive stretch, the resistance disappears. The spinal exion (B) re exes result in exion across multiple joints to withdraw from painful stimuli and may be exaggerated in states of spasticity. The stretch re ex (F) is the fam iliar m yot act ic re ex (ten d on jerk) as occu rs w it h t ap p ing on t h e kn ee with a hammer. The stretch re ex occurs due to th e activation of th e m u scle spindle and nuclear bag bers causing re ex contraction of skeletal m uscle bers via a monosynaptic pathway—the stretch re ex has both a phasic and tonic component. 3,8,9

Answer 31

A. Clasp-knife response B. Flexion re ex C. F response D. H response E. M response **F. Stretch reflex** ## Footnote Th e H re ex (Ho m an’s [D]) is the electrical equivalent of the tendon re ex circuit and represents the activation of a m uscle contraction w ith subm aximal stimulation insu cient to illicit a direct motor response—the response is m ediated by the activation of m uscle spindles and involves both the dorsal and ventral horns. The H re ex (D) is particularly useful in the diagnosis of S1 rad icu lop at hy. Th e F w ave (C) is evoked by supramaximal stimulus of a mixed motor-sensory nerve and consists of a small muscle action potential recorded after the direct motor response. The F w ave resu lt s from an t id rom ic impulses traveling up the m otor nerve to the anterior horn causing an orthodromic response recorded in distal muscle. A normal F w ave and absent H re ex occur in diseases of sensory nerves and roots. The M w ave (E) is the direct motor response caused by stimulation of a motor nerve. A clasp-knife response consists of the following: if muscles are briskly stretched, the limb moves freely for a short distance followed by rapid resistance—with increasing passive stretch, the resistance disappears. The spinal exion (B) re exes result in exion across multiple joints to withdraw from painful stimuli and may be exaggerated in states of spasticity. The stretch re ex (F) is the fam iliar m yot act ic re ex (ten d on jerk) as occu rs w it h t ap p ing on t h e kn ee with a hammer. The stretch re ex occurs due to th e activation of th e m u scle spindle and nuclear bag bers causing re ex contraction of skeletal m uscle bers via a monosynaptic pathway—the stretch re ex has both a phasic and tonic component. 3,8,9

Answer 32

A. Clasp-knife response **B. Flexion re ex** C. F response D. H response E. M response F. Stretch reflex ## Footnote Th e H re ex (Ho m an’s [D]) is the electrical equivalent of the tendon re ex circuit and represents the activation of a m uscle contraction w ith subm aximal stimulation insu cient to illicit a direct motor response—the response is m ediated by the activation of m uscle spindles and involves both the dorsal and ventral horns. The H re ex (D) is particularly useful in the diagnosis of S1 rad icu lop at hy. Th e F w ave (C) is evoked by supramaximal stimulus of a mixed motor-sensory nerve and consists of a small muscle action potential recorded after the direct motor response. The F w ave resu lt s from an t id rom ic impulses traveling up the m otor nerve to the anterior horn causing an orthodromic response recorded in distal muscle. A normal F w ave and absent H re ex occur in diseases of sensory nerves and roots. The M w ave (E) is the direct motor response caused by stimulation of a motor nerve. A clasp-knife response consists of the following: if muscles are briskly stretched, the limb moves freely for a short distance followed by rapid resistance—with increasing passive stretch, the resistance disappears. The spinal exion (B) re exes result in exion across multiple joints to withdraw from painful stimuli and may be exaggerated in states of spasticity. The stretch re ex (F) is the fam iliar m yot act ic re ex (ten d on jerk) as occu rs w it h t ap p ing on t h e kn ee with a hammer. The stretch re ex occurs due to th e activation of th e m u scle spindle and nuclear bag bers causing re ex contraction of skeletal m uscle bers via a monosynaptic pathway—the stretch re ex has both a phasic and tonic component. 3,8,9

Answer 33

A. Clasp-knife response B. Flexion re ex C. F response **D. H response** E. M response F. Stretch reflex ## Footnote Th e H re ex (Ho m an’s [D]) is the electrical equivalent of the tendon re ex circuit and represents the activation of a m uscle contraction w ith subm aximal stimulation insu cient to illicit a direct motor response—the response is m ediated by the activation of m uscle spindles and involves both the dorsal and ventral horns. The H re ex (D) is particularly useful in the diagnosis of S1 rad icu lop at hy. Th e F w ave (C) is evoked by supramaximal stimulus of a mixed motor-sensory nerve and consists of a small muscle action potential recorded after the direct motor response. The F w ave resu lt s from an t id rom ic impulses traveling up the m otor nerve to the anterior horn causing an orthodromic response recorded in distal muscle. A normal F w ave and absent H re ex occur in diseases of sensory nerves and roots. The M w ave (E) is the direct motor response caused by stimulation of a motor nerve. A clasp-knife response consists of the following: if muscles are briskly stretched, the limb moves freely for a short distance followed by rapid resistance—with increasing passive stretch, the resistance disappears. The spinal exion (B) re exes result in exion across multiple joints to withdraw from painful stimuli and may be exaggerated in states of spasticity. The stretch re ex (F) is the fam iliar m yot act ic re ex (ten d on jerk) as occu rs w it h t ap p ing on t h e kn ee with a hammer. The stretch re ex occurs due to th e activation of th e m u scle spindle and nuclear bag bers causing re ex contraction of skeletal m uscle bers via a monosynaptic pathway—the stretch re ex has both a phasic and tonic component. 3,8,9

Answer 34

A. Clasp-knife response B. Flexion re ex C. F response D. H response **E. M response** F. Stretch reflex ## Footnote Th e H re ex (Ho m an’s [D]) is the electrical equivalent of the tendon re ex circuit and represents the activation of a m uscle contraction w ith subm aximal stimulation insu cient to illicit a direct motor response—the response is m ediated by the activation of m uscle spindles and involves both the dorsal and ventral horns. The H re ex (D) is particularly useful in the diagnosis of S1 rad icu lop at hy. Th e F w ave (C) is evoked by supramaximal stimulus of a mixed motor-sensory nerve and consists of a small muscle action potential recorded after the direct motor response. The F w ave resu lt s from an t id rom ic impulses traveling up the m otor nerve to the anterior horn causing an orthodromic response recorded in distal muscle. A normal F w ave and absent H re ex occur in diseases of sensory nerves and roots. The M w ave (E) is the direct motor response caused by stimulation of a motor nerve. A clasp-knife response consists of the following: if muscles are briskly stretched, the limb moves freely for a short distance followed by rapid resistance—with increasing passive stretch, the resistance disappears. The spinal exion (B) re exes result in exion across multiple joints to withdraw from painful stimuli and may be exaggerated in states of spasticity. The stretch re ex (F) is the fam iliar m yot act ic re ex (ten d on jerk) as occu rs w it h t ap p ing on t h e kn ee with a hammer. The stretch re ex occurs due to th e activation of th e m u scle spindle and nuclear bag bers causing re ex contraction of skeletal m uscle bers via a monosynaptic pathway—the stretch re ex has both a phasic and tonic component. 3,8,9

Answer 35

**A. Clasp-knife response** B. Flexion re ex C. F response D. H response E. M response F. Stretch reflex ## Footnote Th e H re ex (Ho m an’s [D]) is the electrical equivalent of the tendon re ex circuit and represents the activation of a m uscle contraction w ith subm aximal stimulation insu cient to illicit a direct motor response—the response is m ediated by the activation of m uscle spindles and involves both the dorsal and ventral horns. The H re ex (D) is particularly useful in the diagnosis of S1 rad icu lop at hy. Th e F w ave (C) is evoked by supramaximal stimulus of a mixed motor-sensory nerve and consists of a small muscle action potential recorded after the direct motor response. The F w ave resu lt s from an t id rom ic impulses traveling up the m otor nerve to the anterior horn causing an orthodromic response recorded in distal muscle. A normal F w ave and absent H re ex occur in diseases of sensory nerves and roots. The M w ave (E) is the direct motor response caused by stimulation of a motor nerve. A clasp-knife response consists of the following: if muscles are briskly stretched, the limb moves freely for a short distance followed by rapid resistance—with increasing passive stretch, the resistance disappears. The spinal exion (B) re exes result in exion across multiple joints to withdraw from painful stimuli and may be exaggerated in states of spasticity. The stretch re ex (F) is the fam iliar m yot act ic re ex (ten d on jerk) as occu rs w it h t ap p ing on t h e kn ee with a hammer. The stretch re ex occurs due to th e activation of th e m u scle spindle and nuclear bag bers causing re ex contraction of skeletal m uscle bers via a monosynaptic pathway—the stretch re ex has both a phasic and tonic component. 3,8,9

Answer 36

A. Parasympathetic bers from T9 to L1 **B. Parasympathetic bers from S2 to S4** C. Sympathetic bers from T9 to L1 D. Sympathetic bers from S2 to S4 E. Pudendal nerves ## Footnote Th e d et r u sor m u scle of t h e b la d d e r is in n e r vat e d by parasympathetic bers from the S2-S4 (B) n er ve roots. 9

Answer 37

A. Chromatolysis is always associated with decreased protein synthesis. B. Retraction bulbs form only at the proximal end of the cut nerve. **C. Terminal degeneration leads to the loss of presynaptic terminals.** D. Wallerian degeneration occurs before terminal degeneration. E. Wallerian degeneration leads to loss of the proximal axon segment. ## Footnote Ch r o m a t o lys is is a s s o c ia t e d w it h increased protein synthesis (A is false). Re t r a c t io n b u lb s , fr o m t h e b u ild u p o f t r a n s p o r t e d m a t e r ia ls , o cc u r a t both the proximal and the distal ends of the cut nerve (B is false). Waller ian degeneration begins in the distal end of the axon 1 week after initial degenerative changes begin in the axon terminal (D and E are false). Te r m i n a l d e g e n e r a t i o n d o e s l e a d t o t h e loss of presynaptic terminals (C). 8

Answer 38

A. I, II, III **B. I, III** C. II, IV D. IV E. All of the above ## Footnote Ca rb o n d i o x i d e and volatile anesthetic agents increase cerebrospinal uid (CSF) production, whereas carbonic anhydrase inhibitors and norepinephrine in h ibit CSF production . 10

Answer 39

A. Acetylcholine B. GABA C. Glutamate **D. Glycine** E. Histamine ## Footnote Re n s h a w ce lls a r e in h ib it o r y in t e r n e u r o n s lo c a t e d in t h e ve n t r a l h o r n a n d are responsible for a negative feedback re ex called recurrent inhibition. Re n s h a w ce lls u s e g lyc in e a s t h e ir p r in c ip le n e u r o t r a n s m it t e r. 6

Answer 40

**A. Wave I** B. Wave II C. Wave III D. Wave IV E. Wave V ## Footnote St im u la t io n o f t h e co ch le a r n e r ve b y click s d elive r e d t o t h e e a r ca u s e s t h e appearance of seven waves as recorded by scalp electrodes—brainstem auditory evoked responses (BAERs). Wave I represents activation of the auditory nerve. Wave II represents activation of the cochlear nucleus. Wave III represents activation of the superior olivary nucleus. Wave IV represents activation of the lateral lem niscus. Wave V represents activation of the inferior colliculus. Wave VI corresponds to the medial geniculate nucleus. Wave VII corresponds to the auditory radiations. 9

Answer 41

A. Wave I **B. Wave II** C. Wave III D. Wave IV E. Wave V ## Footnote St im u la t io n o f t h e co ch le a r n e r ve b y click s d elive r e d t o t h e e a r ca u s e s t h e appearance of seven waves as recorded by scalp electrodes—brainstem auditory evoked responses (BAERs). Wave I represents activation of the auditory nerve. Wave II represents activation of the cochlear nucleus. Wave III represents activation of the superior olivary nucleus. Wave IV represents activation of the lateral lem niscus. Wave V represents activation of the inferior colliculus. Wave VI corresponds to the medial geniculate nucleus. Wave VII corresponds to the auditory radiations. 9

Answer 42

A. Wave I B. Wave II C. Wave III D. Wave IV **E. Wave V** ## Footnote St im u la t io n o f t h e co ch le a r n e r ve b y click s d elive r e d t o t h e e a r ca u s e s t h e appearance of seven waves as recorded by scalp electrodes—brainstem auditory evoked responses (BAERs). Wave I represents activation of the auditory nerve. Wave II represents activation of the cochlear nucleus. Wave III represents activation of the superior olivary nucleus. Wave IV represents activation of the lateral lem niscus. Wave V represents activation of the inferior colliculus. Wave VI corresponds to the medial geniculate nucleus. Wave VII corresponds to the auditory radiations. 9

Answer 43

A. Wave I B. Wave II C. Wave III **D. Wave IV** E. Wave V ## Footnote St im u la t io n o f t h e co ch le a r n e r ve b y click s d elive r e d t o t h e e a r ca u s e s t h e appearance of seven waves as recorded by scalp electrodes—brainstem auditory evoked responses (BAERs). Wave I represents activation of the auditory nerve. Wave II represents activation of the cochlear nucleus. Wave III represents activation of the superior olivary nucleus. Wave IV represents activation of the lateral lem niscus. Wave V represents activation of the inferior colliculus. Wave VI corresponds to the medial geniculate nucleus. Wave VII corresponds to the auditory radiations. 9

Answer 44

A. Wave I B. Wave II **C. Wave III** D. Wave IV E. Wave V ## Footnote St im u la t io n o f t h e co ch le a r n e r ve b y click s d elive r e d t o t h e e a r ca u s e s t h e appearance of seven waves as recorded by scalp electrodes—brainstem auditory evoked responses (BAERs). Wave I represents activation of the auditory nerve. Wave II represents activation of the cochlear nucleus. Wave III represents activation of the superior olivary nucleus. Wave IV represents activation of the lateral lem niscus. Wave V represents activation of the inferior colliculus. Wave VI corresponds to the medial geniculate nucleus. Wave VII corresponds to the auditory radiations. 9

Answer 45

A. Erb’s point **B. N11** C. N13/P13 D. N19 E. P22 ## Footnote Som at ose n sor y evoke d p ot e n t ia ls (SSEPs) in volve t h e a p p licat ion of 5 - p e r second transcutaneous stimuli to the median, peroneal, and tibial nerves, and recording the evoked potentials as they pass the brachial plexus 2–3 cm above the clavicle (Erb’s point [A]), over the C2 vertebra, and over the contralateral parietal cortex. A delay between the peripheral stimulus and Erb ’s p o i n t (A) suggests a peripheral lesion. Absence or delay in N11 (B) im p lies cer vical cord disease. The summated wave that is recorded at the cervicomedullary junction is N13/P13 (C). Th e cor t ical p oten t ial record ed at th e cor tex from m ed ian nerve stimulation is N19/P22 (D and E). Th e cor t ical w ave after t ibial or p ero neal stimulation is N/P 37. 9

Answer 46

**A. Erb’s point** B. N11 C. N13/P13 D. N19 E. P22 ## Footnote Som at ose n sor y evoke d p ot e n t ia ls (SSEPs) in volve t h e a p p licat ion of 5 - p e r second transcutaneous stimuli to the median, peroneal, and tibial nerves, and recording the evoked potentials as they pass the brachial plexus 2–3 cm above the clavicle (Erb’s point [A]), over the C2 vertebra, and over the contralateral parietal cortex. A delay between the peripheral stimulus and Erb ’s p o i n t (A) suggests a peripheral lesion. Absence or delay in N11 (B) im p lies cer vical cord disease. The summated wave that is recorded at the cervicomedullary junction is N13/P13 (C). Th e cor t ical p oten t ial record ed at th e cor tex from m ed ian nerve stimulation is N19/P22 (D and E). Th e cor t ical w ave after t ibial or p ero neal stimulation is N/P 37. 9

Answer 47

A. Erb’s point B. N11 **C. N13/P13** D. N19 E. P22 ## Footnote Som at ose n sor y evoke d p ot e n t ia ls (SSEPs) in volve t h e a p p licat ion of 5 - p e r second transcutaneous stimuli to the median, peroneal, and tibial nerves, and recording the evoked potentials as they pass the brachial plexus 2–3 cm above the clavicle (Erb’s point [A]), over the C2 vertebra, and over the contralateral parietal cortex. A delay between the peripheral stimulus and Erb ’s p o i n t (A) suggests a peripheral lesion. Absence or delay in N11 (B) im p lies cer vical cord disease. The summated wave that is recorded at the cervicomedullary junction is N13/P13 (C). Th e cor t ical p oten t ial record ed at th e cor tex from m ed ian nerve stimulation is N19/P22 (D and E). Th e cor t ical w ave after t ibial or p ero neal stimulation is N/P 37. 9

Answer 48

**A. Erb’s point** B. N11 C. N13/P13 D. N19 E. P22 ## Footnote Som at ose n sor y evoke d p ot e n t ia ls (SSEPs) in volve t h e a p p licat ion of 5 - p e r second transcutaneous stimuli to the median, peroneal, and tibial nerves, and recording the evoked potentials as they pass the brachial plexus 2–3 cm above the clavicle (Erb’s point [A]), over the C2 vertebra, and over the contralateral parietal cortex. A delay between the peripheral stimulus and Erb ’s p o i n t (A) suggests a peripheral lesion. Absence or delay in N11 (B) im p lies cer vical cord disease. The summated wave that is recorded at the cervicomedullary junction is N13/P13 (C). Th e cor t ical p oten t ial record ed at th e cor tex from m ed ian nerve stimulation is N19/P22 (D and E). Th e cor t ical w ave after t ibial or p ero neal stimulation is N/P 37. 9

Answer 49

A. 75 mL/100 g/min B. 55 mL/100 g/min **C. 23 mL/100 g/min** D. 17 mL/100 g/min E. 8 mL/100 g/min ## Footnote Norm al cerebral blood ow is 55 mL/100 g/min (B). Flow red u ct ion below 8–10 mL/100 g/min (E) results in irreversible cerebral infarction. Functional impairm ent occurs at a cerebral blood ow of 23 mL/100 g/min (C). Th e bio chem ical abnorm alities, including depletion of ATP and creatine phosphate and increase of K 1 level (from inju red cells), can be reversed if ad equ ate blood ow is restored in a timely fashion. 9

Answer 50

A. 75 mL/100 g/min B. 55 mL/100 g/min C. 23 mL/100 g/min D. 17 mL/100 g/min **E. 8 mL/100 g/min** ## Footnote Norm al cerebral blood ow is 55 mL/100 g/min (B). Flow red u ct ion below 8–10 mL/100 g/min (E) results in irreversible cerebral infarction. Functional impairm ent occurs at a cerebral blood ow of 23 mL/100 g/min (C). Th e bio chem ical abnorm alities, including depletion of ATP and creatine phosphate and increase of K 1 level (from inju red cells), can be reversed if ad equ ate blood ow is restored in a timely fashion. 9

Answer 51

A. 75 mL/100 g/min **B. 55 mL/100 g/min** C. 23 mL/100 g/min D. 17 mL/100 g/min E. 8 mL/100 g/min ## Footnote Norm al cerebral blood ow is 55 mL/100 g/min (B). Flow red u ct ion below 8–10 mL/100 g/min (E) results in irreversible cerebral infarction. Functional impairm ent occurs at a cerebral blood ow of 23 mL/100 g/min (C). Th e bio chem ical abnorm alities, including depletion of ATP and creatine phosphate and increase of K 1 level (from inju red cells), can be reversed if ad equ ate blood ow is restored in a timely fashion. 9

Answer 52

A. Basket cells B. Golgi cells **C. Granule cells** D. Purkinje cells E. Stellate cells ## Footnote Th e ce reb ellar cor t ex con sist s of t h re e laye r s t h at con t a in ve cell t yp es. Th e molecular layer (outermost) is composed of the axons of the granule cells (C) (parallel bers), stellate (E) and basket cells (A) (interneurons), and dendrites of the underlying Purkinje cells (D). Th e Pu rkinje cell layer (m id d le) contains the cell bodies of the Purkinje neurons. They are the sole output of the cerebellar cortex and are inhibitory. The granular (innermost) layer contains num erous granule cells (C, excitatory; utilize glutamate), a few Go l g i c e l l s ( B) , an d glom er u li (w h ere cells in t h e gran u lar layer form com p lex synaptic contacts with the incoming mossy bers). A erents to the cortex terminate either in the granule cell layer as mossy bers or on the dendrites of Purkinje cells as climbing bers. Both mossy and climbing ber inputs are excitatory to both the deep cerebellar nuclei and the cortex. Stellate (E) and basket cells (A) directly inhibit Purkinje (D) and Go l g i c e l l s ( B) , an d Golgi cells inhibit granule cells (C). 8

Answer 53

A. Basket cells **B. Golgi cells** C. Granule cells D. Purkinje cells E. Stellate cells ## Footnote Th e ce reb ellar cor t ex con sist s of t h re e laye r s t h at con t a in ve cell t yp es. Th e molecular layer (outermost) is composed of the axons of the granule cells (C) (parallel bers), stellate (E) and basket cells (A) (interneurons), and dendrites of the underlying Purkinje cells (D). Th e Pu rkinje cell layer (m id d le) contains the cell bodies of the Purkinje neurons. They are the sole output of the cerebellar cortex and are inhibitory. The granular (innermost) layer contains num erous granule cells (C, excitatory; utilize glutamate), a few Go l g i c e l l s ( B) , an d glom er u li (w h ere cells in t h e gran u lar layer form com p lex synaptic contacts with the incoming mossy bers). A erents to the cortex terminate either in the granule cell layer as mossy bers or on the dendrites of Purkinje cells as climbing bers. Both mossy and climbing ber inputs are excitatory to both the deep cerebellar nuclei and the cortex. Stellate (E) and basket cells (A) directly inhibit Purkinje (D) and Go l g i c e l l s ( B) , an d Golgi cells inhibit granule cells (C). 8

Answer 54

A. Basket cells B. Golgi cells **C. Granule cells** D. Purkinje cells E. Stellate cells ## Footnote Th e ce reb ellar cor t ex con sist s of t h re e laye r s t h at con t a in ve cell t yp es. Th e molecular layer (outermost) is composed of the axons of the granule cells (C) (parallel bers), stellate (E) and basket cells (A) (interneurons), and dendrites of the underlying Purkinje cells (D). Th e Pu rkinje cell layer (m id d le) contains the cell bodies of the Purkinje neurons. They are the sole output of the cerebellar cortex and are inhibitory. The granular (innermost) layer contains num erous granule cells (C, excitatory; utilize glutamate), a few Go l g i c e l l s ( B) , an d glom er u li (w h ere cells in t h e gran u lar layer form com p lex synaptic contacts with the incoming mossy bers). A erents to the cortex terminate either in the granule cell layer as mossy bers or on the dendrites of Purkinje cells as climbing bers. Both mossy and climbing ber inputs are excitatory to both the deep cerebellar nuclei and the cortex. Stellate (E) and basket cells (A) directly inhibit Purkinje (D) and Go l g i c e l l s ( B) , an d Golgi cells inhibit granule cells (C). 8

Answer 55

A. Basket cells B. Golgi cells **C. Granule cells** D. Purkinje cells E. Stellate cells ## Footnote Th e ce reb ellar cor t ex con sist s of t h re e laye r s t h at con t a in ve cell t yp es. Th e molecular layer (outermost) is composed of the axons of the granule cells (C) (parallel bers), stellate (E) and basket cells (A) (interneurons), and dendrites of the underlying Purkinje cells (D). Th e Pu rkinje cell layer (m id d le) contains the cell bodies of the Purkinje neurons. They are the sole output of the cerebellar cortex and are inhibitory. The granular (innermost) layer contains num erous granule cells (C, excitatory; utilize glutamate), a few Go l g i c e l l s ( B) , an d glom er u li (w h ere cells in t h e gran u lar layer form com p lex synaptic contacts with the incoming mossy bers). A erents to the cortex terminate either in the granule cell layer as mossy bers or on the dendrites of Purkinje cells as climbing bers. Both mossy and climbing ber inputs are excitatory to both the deep cerebellar nuclei and the cortex. Stellate (E) and basket cells (A) directly inhibit Purkinje (D) and Go l g i c e l l s ( B) , an d Golgi cells inhibit granule cells (C). 8

Answer 56

A. Basket cells B. Golgi cells C. Granule cells **D. Purkinje cells** E. Stellate cells ## Footnote Th e ce reb ellar cor t ex con sist s of t h re e laye r s t h at con t a in ve cell t yp es. Th e molecular layer (outermost) is composed of the axons of the granule cells (C) (parallel bers), stellate (E) and basket cells (A) (interneurons), and dendrites of the underlying Purkinje cells (D). Th e Pu rkinje cell layer (m id d le) contains the cell bodies of the Purkinje neurons. They are the sole output of the cerebellar cortex and are inhibitory. The granular (innermost) layer contains num erous granule cells (C, excitatory; utilize glutamate), a few Go l g i c e l l s ( B) , an d glom er u li (w h ere cells in t h e gran u lar layer form com p lex synaptic contacts with the incoming mossy bers). A erents to the cortex terminate either in the granule cell layer as mossy bers or on the dendrites of Purkinje cells as climbing bers. Both mossy and climbing ber inputs are excitatory to both the deep cerebellar nuclei and the cortex. Stellate (E) and basket cells (A) directly inhibit Purkinje (D) and Go l g i c e l l s ( B) , an d Golgi cells inhibit granule cells (C). 8

Answer 57

A. Basket cells B. Golgi cells C. Granule cells **D. Purkinje cells** E. Stellate cells ## Footnote Th e ce reb ellar cor t ex con sist s of t h re e laye r s t h at con t a in ve cell t yp es. Th e molecular layer (outermost) is composed of the axons of the granule cells (C) (parallel bers), stellate (E) and basket cells (A) (interneurons), and dendrites of the underlying Purkinje cells (D). Th e Pu rkinje cell layer (m id d le) contains the cell bodies of the Purkinje neurons. They are the sole output of the cerebellar cortex and are inhibitory. The granular (innermost) layer contains num erous granule cells (C, excitatory; utilize glutamate), a few Go l g i c e l l s ( B) , an d glom er u li (w h ere cells in t h e gran u lar layer form com p lex synaptic contacts with the incoming mossy bers). A erents to the cortex terminate either in the granule cell layer as mossy bers or on the dendrites of Purkinje cells as climbing bers. Both mossy and climbing ber inputs are excitatory to both the deep cerebellar nuclei and the cortex. Stellate (E) and basket cells (A) directly inhibit Purkinje (D) and Go l g i c e l l s ( B) , an d Golgi cells inhibit granule cells (C). 8

Answer 58

**A. Basket cells** B. Golgi cells C. Granule cells D. Purkinje cells E. Stellate cells ## Footnote Th e ce reb ellar cor t ex con sist s of t h re e laye r s t h at con t a in ve cell t yp es. Th e molecular layer (outermost) is composed of the axons of the granule cells (C) (parallel bers), stellate (E) and basket cells (A) (interneurons), and dendrites of the underlying Purkinje cells (D). Th e Pu rkinje cell layer (m id d le) contains the cell bodies of the Purkinje neurons. They are the sole output of the cerebellar cortex and are inhibitory. The granular (innermost) layer contains num erous granule cells (C, excitatory; utilize glutamate), a few Go l g i c e l l s ( B) , an d glom er u li (w h ere cells in t h e gran u lar layer form com p lex synaptic contacts with the incoming mossy bers). A erents to the cortex terminate either in the granule cell layer as mossy bers or on the dendrites of Purkinje cells as climbing bers. Both mossy and climbing ber inputs are excitatory to both the deep cerebellar nuclei and the cortex. Stellate (E) and basket cells (A) directly inhibit Purkinje (D) and Go l g i c e l l s ( B) , an d Golgi cells inhibit granule cells (C). 8

Answer 59

A. Basket cells B. Golgi cells **C. Granule cells** D. Purkinje cells E. Stellate cells ## Footnote Th e ce reb ellar cor t ex con sist s of t h re e laye r s t h at con t a in ve cell t yp es. Th e molecular layer (outermost) is composed of the axons of the granule cells (C) (parallel bers), stellate (E) and basket cells (A) (interneurons), and dendrites of the underlying Purkinje cells (D). Th e Pu rkinje cell layer (m id d le) contains the cell bodies of the Purkinje neurons. They are the sole output of the cerebellar cortex and are inhibitory. The granular (innermost) layer contains num erous granule cells (C, excitatory; utilize glutamate), a few Go l g i c e l l s ( B) , an d glom er u li (w h ere cells in t h e gran u lar layer form com p lex synaptic contacts with the incoming mossy bers). A erents to the cortex terminate either in the granule cell layer as mossy bers or on the dendrites of Purkinje cells as climbing bers. Both mossy and climbing ber inputs are excitatory to both the deep cerebellar nuclei and the cortex. Stellate (E) and basket cells (A) directly inhibit Purkinje (D) and Go l g i c e l l s ( B) , an d Golgi cells inhibit granule cells (C). 8

Answer 60

**A. The utricular macule is oriented horizontally, and the saccular macule is oriented vertically. ** B. The utricular macule is oriented vertically, and the saccular macule is oriented horizontally. C. They are both oriented horizontally. D. They are both oriented vertically. E. None of the above is true. ## Footnote When the head is upright, the utricular macule is oriented in the horizontal plane and can be activated by linear forces in the horizontal plane. The saccular macule is oriented in the vertical plane and can be stimulated by linear forces in the vertical plane (A is correct). 7

Answer 61

A. Aa fibers B. Ab fibers C. Ag fibers **D. Ad fibers** E. C fibers ## Footnote Nociception is m ediated prim arily by lightly m yelinated free ner ve endings of type Ad bers (D) or unmyelinated C b e r s ( E) . Th e sen sat ion of sh ar p pain is mediated by Ad bers (D). C b e r s ( E) relay information regarding mechanical, thermal, or chemical stimuli. 7

Answer 62

A. Neuronal ACh receptors contain four types of subunits. B. The slow excitatory postsynaptic potential (EPSP) is produced by muscarinic receptors closing Na 1 an d Ca 21 ch an n els w h ile open ing K 1 ch an n els. C. The slow inhibitory postsynaptic potential (IPSP) is mediated by activation of muscarinic receptors that close K 1 ch an n els. **D. The fast EPSP is mediated by nicotinic ACh receptors.** E. Peptides are never co-released with ACh. ## Footnote Un like t h e ACh re ce p t or s at t h e n e u rom u scu lar ju n ct ion , t h e ACh re ce p tor s in autonomic ganglia contain only two types of subunits (A is false). Th e fast excitatory postsynaptic potential (EPSP) is m ediated by nicotinic ACh receptors (D is true), t h e slow EPSP is m ed iated by m u scar in ic receptors op en in g Na 1 and Ca 21 ch a n n els a n d closin g K 1 ch a n n els (B is false), an d t h e slow in h ibitor y postsynaptic potential (IPSP) is mediated by muscarinic receptors that open K 1 ch an n els (C is false). A variet y of p ept id es t h at ap p ear to be m od u lator y in action may be co-released with Ach (E is false). 8

Answer 63

**A. Increased postganglionic sympathetic activity results in bladder wall contraction.** B. Increased postganglionic sympathetic activity results in a -adrenergic inhibition of parasympathetics in the pelvic ganglion. C. Motor neurons in the ventral horn of the sacral spinal cord innervate the external sphincter. D. Parasympathetic activity promotes bladder emptying. E. The internal sphincter is innervated by sympathetic bers. ## Footnote In creased sym p at h et ic act ivit y resu lt s in blad d er w all rela xat ion (A is false). Th e ot h e r resp on ses a re t r u e re ga rd in g in n e r vat ion of t h e u r in a r y syst e m . In creased p ost gan glion ic sym p at h et ic act ivit y resu lt s in a -adrenergic inhibition of parasympathetics in the pelvic ganglion (B), m otor n eu ron s in t h e ventral horn of the sacral spinal cord innervate the external sphincter (C), parasympathetic activity promotes bladder emptying (D), an d t h e in ter n al sphincter is innervated by sympathetic bers (E). 7

Answer 64

A. I, II, III **B. I, III** C. II, IV D. IV E. All of the above ## Footnote Fib e r s fr o m t h e su p e r io r sa livat o r y n u cle u s t r avel w it h t h e fa cia l n e r ve reaching either the pterygopalatine ganglion via the GSPN and vidian nerve or the submandibular ganglion via the chorda tympani nerve. The geniculate ganglion contains the cell bodies of pseudounipolar neurons carrying a erent inform ation in the facial nerve. The trigem inal ganglion houses the cell bodies of pseudounipolar neurons carrying a erent information in the trigeminal nerve. 7

Answer 65

A. I and II **B. II and III** C. III and IV D. IV and V E. V and VI ## Footnote Ip silat eral cor t ico -cor t ical associat ion bers ar ise from cells in cor t ical layers II and III. Cells that give rise to commissural bers that interconnect homologous cortical areas via the corpus callosum are found in layer III of the cerebral cortex (the external pyramidal layer). La y e r I is the plexiform molecular layer and consists mainly of nerve cell processes. La y e r II is the external granular layer comprised mostly of small granule cells and projects primarily to local or distant cortical areas as association bers. La y e r IV, t h e internal granular layer, is important for a erent signaling and is thicker in the primary sensory area. La y e r V, t h e in ter n al pyram id al layer, is t h e sou rce of the majority of output bers for the cerebral cortex. La y e r VI is the fusiform layer and lies adjacent to underlying w hite m atter and consists prim arily of association neurons. 7

Answer 66

A. Both EPSP and IPSP decrease B. Both EPSP and IPSP increase **C. EPSP decreases and IPSP increases** D. EPSP increases and IPSP decreases E. There is no change in IPSP, but EPSP increases ## Footnote As t h e m e m b r a n e o f a m ot o r n e u r o n b e co m e s in cr e a s in gly d e p o la r ize d , excitatory postsynaptic potentials decrease while inhibitory postsynaptic potentials increase. Ch o i c e C is correct. 8

Answer 67

A. They are part of a negative feedback loop to the motor neurons. **B. They facilitate Ia inhibitory interneurons that act on antagonist motor neurons.** C. They inhibit motor neurons that innervate synergist muscles. D. They make divergent connections to motor neurons. E. They receive input from descending pathways. ## Footnote Re n s h a w ce lls a r e lo c a t e d in t h e a n t e r io r h o r n a n d p a r t ic ip a t e in a n e ga t ive feed back loop to t h e m otor n eu ron s (A). They receive input from descending pathways (E), m ake d ivergen t con n ect ion s to m otor n eu ron s (D), an d in h ibit motor neurons that inhibit synergistic muscles (C). Du ring d evelop m en t , Re n s h a w ce lls r e ce ive in p u t fr o m Ia a e r e n t s , b u t t h e y p r o je c t t o a motor neurons (B is false). 3,6,8

Answer 68

A. Inferior vestibular nucleus **B. Lateral vestibular nucleus** C. Medial vestibular nucleus D. Superior vestibular nucleus E. None of the above ## Footnote Par t of th e lateral vestibulospinal nucleus (Deiters’ nucleus [B]) receives direct inhibitory input from Purkinje cells in the cerebellar vermis. Decerebrate rigidity is exacerbated if the portion of the cerebellum connected to Deiters’ nucleus (B) is interrupted because of removal of this inhibitory action. The lateral vestibulospinal tract (B) has a facilitatory e ect on both a and γ neurons that innervate m uscles in the lim bs; this tonic excitation of the extensors of the leg and the exors of the arm helps in the maintenance of posture. The superior and medial vestibular nuclei (D) receive sensory input from the sem icircular canals via the vestibular nerve and project to the medial longitudinal fasciculus and medial vestibulospinal tract to mediate re exes of both ocular and head movements in response to vestibular stimuli. Th e inferior vestibular nucleus (A) receives a erents from the sem icircular canals and utricle and sends its projections to the reticular form ation and cerebellum , acting as an integration center for the vestibular labyrinth and cerebellum

Answer 69

A. Inferior vestibular nucleus B. Lateral vestibular nucleus C. Medial vestibular nucleus **D. Superior vestibular nucleus** E. None of the above ## Footnote Par t of th e lateral vestibulospinal nucleus (Deiters’ nucleus [B]) receives direct inhibitory input from Purkinje cells in the cerebellar vermis. Decerebrate rigidity is exacerbated if the portion of the cerebellum connected to Deiters’ nucleus (B) is interrupted because of removal of this inhibitory action. The lateral vestibulospinal tract (B) has a facilitatory e ect on both a and γ neurons that innervate m uscles in the lim bs; this tonic excitation of the extensors of the leg and the exors of the arm helps in the maintenance of posture. The superior and medial vestibular nuclei (D) receive sensory input from the sem icircular canals via the vestibular nerve and project to the medial longitudinal fasciculus and medial vestibulospinal tract to mediate re exes of both ocular and head movements in response to vestibular stimuli. Th e inferior vestibular nucleus (A) receives a erents from the sem icircular canals and utricle and sends its projections to the reticular form ation and cerebellum , acting as an integration center for the vestibular labyrinth and cerebellum

Answer 70

A. Inferior vestibular nucleus **B. Lateral vestibular nucleus** C. Medial vestibular nucleus D. Superior vestibular nucleus E. None of the above ## Footnote Par t of th e lateral vestibulospinal nucleus (Deiters’ nucleus [B]) receives direct inhibitory input from Purkinje cells in the cerebellar vermis. Decerebrate rigidity is exacerbated if the portion of the cerebellum connected to Deiters’ nucleus (B) is interrupted because of removal of this inhibitory action. The lateral vestibulospinal tract (B) has a facilitatory e ect on both a and γ neurons that innervate m uscles in the lim bs; this tonic excitation of the extensors of the leg and the exors of the arm helps in the maintenance of posture. The superior and medial vestibular nuclei (D) receive sensory input from the sem icircular canals via the vestibular nerve and project to the medial longitudinal fasciculus and medial vestibulospinal tract to mediate re exes of both ocular and head movements in response to vestibular stimuli. Th e inferior vestibular nucleus (A) receives a erents from the sem icircular canals and utricle and sends its projections to the reticular form ation and cerebellum , acting as an integration center for the vestibular labyrinth and cerebellum

Answer 71

**A. Inferior vestibular nucleus** B. Lateral vestibular nucleus C. Medial vestibular nucleus D. Superior vestibular nucleus E. None of the above ## Footnote Par t of th e lateral vestibulospinal nucleus (Deiters’ nucleus [B]) receives direct inhibitory input from Purkinje cells in the cerebellar vermis. Decerebrate rigidity is exacerbated if the portion of the cerebellum connected to Deiters’ nucleus (B) is interrupted because of removal of this inhibitory action. The lateral vestibulospinal tract (B) has a facilitatory e ect on both a and γ neurons that innervate m uscles in the lim bs; this tonic excitation of the extensors of the leg and the exors of the arm helps in the maintenance of posture. The superior and medial vestibular nuclei (D) receive sensory input from the sem icircular canals via the vestibular nerve and project to the medial longitudinal fasciculus and medial vestibulospinal tract to mediate re exes of both ocular and head movements in response to vestibular stimuli. Th e inferior vestibular nucleus (A) receives a erents from the sem icircular canals and utricle and sends its projections to the reticular form ation and cerebellum , acting as an integration center for the vestibular labyrinth and cerebellum

Answer 72

A. Inferior vestibular nucleus **B. Lateral vestibular nucleus** C. Medial vestibular nucleus D. Superior vestibular nucleus E. None of the above ## Footnote Par t of th e lateral vestibulospinal nucleus (Deiters’ nucleus [B]) receives direct inhibitory input from Purkinje cells in the cerebellar vermis. Decerebrate rigidity is exacerbated if the portion of the cerebellum connected to Deiters’ nucleus (B) is interrupted because of removal of this inhibitory action. The lateral vestibulospinal tract (B) has a facilitatory e ect on both a and γ neurons that innervate m uscles in the lim bs; this tonic excitation of the extensors of the leg and the exors of the arm helps in the maintenance of posture. The superior and medial vestibular nuclei (D) receive sensory input from the sem icircular canals via the vestibular nerve and project to the medial longitudinal fasciculus and medial vestibulospinal tract to mediate re exes of both ocular and head movements in response to vestibular stimuli. Th e inferior vestibular nucleus (A) receives a erents from the sem icircular canals and utricle and sends its projections to the reticular form ation and cerebellum , acting as an integration center for the vestibular labyrinth and cerebellum

Answer 73

A. Attachment of fatty acids B. Formation of O-linked sugars **C. Initiation of N-linked glycosylation** D. Sugar phosphorylation E. Sulfation of tyrosine residues ## Footnote Th e Golgi a p p a r at u s se r ves t w o m ajor fu n ct ion s for t h e p rocessin g of m e m brane proteins: sorting and targeting of proteins, and post-translational modi cations—particularly of oligosaccharide chains that have already been added in the rough endoplasmic reticulum. (The initial steps of N-linked glycosylation take place in the endoplasmic reticulum; C is false.) The other choices listed take place in the Golgi apparatus: attachment of fatty acids (A), form ation of O-linked sugars (B), sugar phosphorylation (D), an d sulfation of tyrosine residues (E). 2,6

Answer 74

**A. Binds to the ACh receptor ** B. Blocks reuptake of dopamine C. Blocks voltage-gated K 1 ch an n els D. Blocks voltage-gated Na 1 ch an n els E. Depletes norepinephrine (NE) from vesicles F. Inhibits GTP hydrolysis G. Prevents presynaptic release of quanta of ACh ## Footnote a -Bungarotoxin (A) is a n e u rotoxin fou n d in sn ake ve n om t h at is sele ct ive for the nicotinic acetylcholine receptor at the muscle end-plate. Bo tu lin u m toxin (G) blocks the release of acetylcholine quanta at the presynaptic membrane. Ch o l e ra t o x i n ( F) inhibits GTP hydrolysis leading to constitutive activity of adenylyl cyclase and increased intracellular cAMP levels. Co c a i n e ( B) acts on the dopamine transporter (DAT) inhibiting dopamine reuptake. Re s e rp i n e (E) interacts w ith adrenergic storage vesicles and inhibits their capacity to concentrate and store norepinephrine and dopam ine. Te t r a e t h y l a m m o n i u m ( C) is an am m onium salt sim ilar to hexam ethonium that functions as a “nicotine paralyzing” ganglion blocker, acting primarily via blockade of voltage-gated K 1 ch a n n els. Te t r o d o t o x i n ( D ) is a sh t oxin t h at b locks Na 1 ch a n n els in e xcit able cells. 2,5,8

Answer 75

A. Binds to the ACh receptor B. Blocks reuptake of dopamine C. Blocks voltage-gated K 1 ch an n els D. Blocks voltage-gated Na 1 ch an n els E. Depletes norepinephrine (NE) from vesicles F. Inhibits GTP hydrolysis **G. Prevents presynaptic release of quanta of ACh** ## Footnote a -Bungarotoxin (A) is a n e u rotoxin fou n d in sn ake ve n om t h at is sele ct ive for the nicotinic acetylcholine receptor at the muscle end-plate. Bo tu lin u m toxin (G) blocks the release of acetylcholine quanta at the presynaptic membrane. Ch o l e ra t o x i n ( F) inhibits GTP hydrolysis leading to constitutive activity of adenylyl cyclase and increased intracellular cAMP levels. Co c a i n e ( B) acts on the dopamine transporter (DAT) inhibiting dopamine reuptake. Re s e rp i n e (E) interacts w ith adrenergic storage vesicles and inhibits their capacity to concentrate and store norepinephrine and dopam ine. Te t r a e t h y l a m m o n i u m ( C) is an am m onium salt sim ilar to hexam ethonium that functions as a “nicotine paralyzing” ganglion blocker, acting primarily via blockade of voltage-gated K 1 ch a n n els. Te t r o d o t o x i n ( D ) is a sh t oxin t h at b locks Na 1 ch a n n els in e xcit able cells. 2,5,8

Answer 76

A. Binds to the ACh receptor B. Blocks reuptake of dopamine C. Blocks voltage-gated K 1 ch an n els D. Blocks voltage-gated Na 1 ch an n els E. Depletes norepinephrine (NE) from vesicles **F. Inhibits GTP hydrolysis ** G. Prevents presynaptic release of quanta of ACh ## Footnote a -Bungarotoxin (A) is a n e u rotoxin fou n d in sn ake ve n om t h at is sele ct ive for the nicotinic acetylcholine receptor at the muscle end-plate. Bo tu lin u m toxin (G) blocks the release of acetylcholine quanta at the presynaptic membrane. Ch o l e ra t o x i n ( F) inhibits GTP hydrolysis leading to constitutive activity of adenylyl cyclase and increased intracellular cAMP levels. Co c a i n e ( B) acts on the dopamine transporter (DAT) inhibiting dopamine reuptake. Re s e rp i n e (E) interacts w ith adrenergic storage vesicles and inhibits their capacity to concentrate and store norepinephrine and dopam ine. Te t r a e t h y l a m m o n i u m ( C) is an am m onium salt sim ilar to hexam ethonium that functions as a “nicotine paralyzing” ganglion blocker, acting primarily via blockade of voltage-gated K 1 ch a n n els. Te t r o d o t o x i n ( D ) is a sh t oxin t h at b locks Na 1 ch a n n els in e xcit able cells. 2,5,8

Answer 77

A. Binds to the ACh receptor **B. Blocks reuptake of dopamine** C. Blocks voltage-gated K 1 ch an n els D. Blocks voltage-gated Na 1 ch an n els E. Depletes norepinephrine (NE) from vesicles F. Inhibits GTP hydrolysis G. Prevents presynaptic release of quanta of ACh ## Footnote a -Bungarotoxin (A) is a n e u rotoxin fou n d in sn ake ve n om t h at is sele ct ive for the nicotinic acetylcholine receptor at the muscle end-plate. Bo tu lin u m toxin (G) blocks the release of acetylcholine quanta at the presynaptic membrane. Ch o l e ra t o x i n ( F) inhibits GTP hydrolysis leading to constitutive activity of adenylyl cyclase and increased intracellular cAMP levels. Co c a i n e ( B) acts on the dopamine transporter (DAT) inhibiting dopamine reuptake. Re s e rp i n e (E) interacts w ith adrenergic storage vesicles and inhibits their capacity to concentrate and store norepinephrine and dopam ine. Te t r a e t h y l a m m o n i u m ( C) is an am m onium salt sim ilar to hexam ethonium that functions as a “nicotine paralyzing” ganglion blocker, acting primarily via blockade of voltage-gated K 1 ch a n n els. Te t r o d o t o x i n ( D ) is a sh t oxin t h at b locks Na 1 ch a n n els in e xcit able cells. 2,5,8

Answer 78

A. Binds to the ACh receptor B. Blocks reuptake of dopamine C. Blocks voltage-gated K 1 ch an n els D. Blocks voltage-gated Na 1 ch an n els **E. Depletes norepinephrine (NE) from vesicles** F. Inhibits GTP hydrolysis G. Prevents presynaptic release of quanta of ACh ## Footnote a -Bungarotoxin (A) is a n e u rotoxin fou n d in sn ake ve n om t h at is sele ct ive for the nicotinic acetylcholine receptor at the muscle end-plate. Bo tu lin u m toxin (G) blocks the release of acetylcholine quanta at the presynaptic membrane. Ch o l e ra t o x i n ( F) inhibits GTP hydrolysis leading to constitutive activity of adenylyl cyclase and increased intracellular cAMP levels. Co c a i n e ( B) acts on the dopamine transporter (DAT) inhibiting dopamine reuptake. Re s e rp i n e (E) interacts w ith adrenergic storage vesicles and inhibits their capacity to concentrate and store norepinephrine and dopam ine. Te t r a e t h y l a m m o n i u m ( C) is an am m onium salt sim ilar to hexam ethonium that functions as a “nicotine paralyzing” ganglion blocker, acting primarily via blockade of voltage-gated K 1 ch a n n els. Te t r o d o t o x i n ( D ) is a sh t oxin t h at b locks Na 1 ch a n n els in e xcit able cells. 2,5,8

Answer 79

A. Binds to the ACh receptor B. Blocks reuptake of dopamine **C. Blocks voltage-gated K 1 ch an n els** D. Blocks voltage-gated Na 1 ch an n els E. Depletes norepinephrine (NE) from vesicles F. Inhibits GTP hydrolysis G. Prevents presynaptic release of quanta of ACh ## Footnote a -Bungarotoxin (A) is a n e u rotoxin fou n d in sn ake ve n om t h at is sele ct ive for the nicotinic acetylcholine receptor at the muscle end-plate. Bo tu lin u m toxin (G) blocks the release of acetylcholine quanta at the presynaptic membrane. Ch o l e ra t o x i n ( F) inhibits GTP hydrolysis leading to constitutive activity of adenylyl cyclase and increased intracellular cAMP levels. Co c a i n e ( B) acts on the dopamine transporter (DAT) inhibiting dopamine reuptake. Re s e rp i n e (E) interacts w ith adrenergic storage vesicles and inhibits their capacity to concentrate and store norepinephrine and dopam ine. Te t r a e t h y l a m m o n i u m ( C) is an am m onium salt sim ilar to hexam ethonium that functions as a “nicotine paralyzing” ganglion blocker, acting primarily via blockade of voltage-gated K 1 ch a n n els. Te t r o d o t o x i n ( D ) is a sh t oxin t h at b locks Na 1 ch a n n els in e xcit able cells. 2,5,8

Answer 80

A. Binds to the ACh receptor B. Blocks reuptake of dopamine C. Blocks voltage-gated K 1 ch an n els **D. Blocks voltage-gated Na 1 channels** E. Depletes norepinephrine (NE) from vesicles F. Inhibits GTP hydrolysis G. Prevents presynaptic release of quanta of ACh ## Footnote a -Bungarotoxin (A) is a neurotoxin found in snake venom that is select ive for the nicot inic acetylcholine receptor at the muscle end-plate. Botulinum toxin (G) blocks the release of acetylcholine quanta at the presynapt ic m embrane. Cholera toxin (F) inhibits GTP hydrolysis leading to constitutive act ivity of adenylyl cyclase and increased intracellular cAMP levels. Cocaine (B) acts on the dopamine t ransporter (DAT) inhibiting dopamine reuptake. Reserpine (E) interacts with adrenergic storage vesicles and inhibits their capacity to concentrate and store norepinephrine and dopamine. Tetraethylammonium (C) is an ammonium salt similar to hexamethonium that funct ions as a “nicot ine paralyzing” ganglion blocker, acting primarily via blockade of voltage-gated K1 channels. Tetrodotoxin (D) is a sh toxin that blocks Na1 channels in excitable cells.2

Answer 81

**A. The electrical force equals the chemical force** B. The net electrical force is zero C. The net chemical force is zero D. There is no movement of K ion s across th e m em bran e E. None of the above ## Footnote At the equilibrium potent ial, the chemical and electrical forces are equal, but opposite (A). There is no net m ovement of K ions across the m embrane (D is false). Neither the net chemical nor the net elect rical force equal zero at the equilibrium potential of potassium (B and C are false).2,11

Answer 82

A. Activation of any G protein will inhibit the activation of other G proteins in the membrane B. Hydrolysis of bound GTP to GDP inactivates a G protein C. The bg su bun it stabilizes th e bin ding of GDP **D. The bg su bun it stabilizes th e bin ding of GTP** E. When activated, the a subun it’s a n it y for th e bg subun it decreases ## Footnote Upon binding of a ligand to a G-protein-coupled receptor, GDP on the a subunit is converted to GTP and the G protein dissociates from the receptor. The a and bg subunits then dissociate (the a subunit’s a nity for the b g subunit decreases [E]). Both subunits are then free to exert their e ects on downstream e ectors, including the inhibit ion of other G proteins in the membrane (A). The a subunit then catalyzes hydrolysis of GTP to GDP, promot ing reassembly of the trimer and receptor inactivation (B). At rest , the bg subunit inhibits activat ion by both stabilizing the binding of GDP (C) and inhibit ing the binding of GTP (D is false).

Answer 83

A. Ampli ed by increased muscle temperature B. Hyperpolarization **C. Not reversed by anticholinesterase agents** D. Not similar to that of decamethonium E. Similar to that of D-tubocurarine ## Footnote Succinylcholine and decamethonium cause depolarizing neuromuscular blockade (B and D are false). The e ect is not reversed by ant icholinesterase agents (C) and is ampli ed by decreased muscle temperature (A is false). Succinylcholine is resistant to the act ion of acet ylcholinesterase (C is true)

Answer 84

A. Area 1 B. Area 2 **C. Area 3a** D. Area 3b

Answer 85

A. Area 1 **B. Area 2** C. Area 3a D. Area 3b

Answer 86

A. Area 1 B. Area 2 C. Area 3a **D. Area 3b**

Answer 87

**A. Area 1** B. Area 2 C. Area 3a D. Area 3b ## Footnote The primary somatosensory area consists of Brodmann’s areas 1, 2, and 3. Area 1 (A) receives input from rapidly adapting receptors in the skin. Area 2 (B) deals w ith pressure and joint position in deep tissues. Area 3a (C) receives muscle, tendon, and joint stretch receptors. Area 3b (D) receives input from both slowly and rapidly adapting receptors in the skin

Answer 88

**A. Proprioception from the leg is relayed in the dorsal columns** B. Second-order neurons cross the midline in the medial lemniscus C. Thalamic neurons project to the primary somatic sensory cortex (SI) D. Thalamic neurons project to the secondary somatic sensory cortex (SII) E. Touch and vibration sense from the arm is relayed in the dorsal columns ## Footnote Proprioception from the leg is relayed in the lateral column by axons of neurons in Clarke’s column (A is false). The other responses regarding the dorsal column medial lemniscal system are true. In addition to sending axons to the primary somatic sensory cortex (SI [C]), thalamic neurons send a sparse project ion to the secondary somat ic sensory cortex (SII [D]). Touch and vibration sense from the arm are relayed in the dorsal columns (E). Second-order neurons cross the midline in the medial lemniscus (B).

Answer 89

A. Cerebellar hemisphere, intermediate part (interposed nuclei) B. Cerebellar hemisphere, lateral part (dentate nuclei) C. Flocculonodular (lateral vestibular nucleus) **D. Vermis (fastigial nucleus)** E. None of the above

Answer 90

**A. Cerebellar hemisphere, intermediate part (interposed nuclei)** B. Cerebellar hemisphere, lateral part (dentate nuclei) C. Flocculonodular (lateral vestibular nucleus) D. Vermis (fastigial nucleus) E. None of the above

Answer 91

A. Cerebellar hemisphere, intermediate part (interposed nuclei) **B. Cerebellar hemisphere, lateral part (dentate nuclei)** C. Flocculonodular (lateral vestibular nucleus) D. Vermis (fastigial nucleus) E. None of the above

Answer 92

A. Cerebellar hemisphere, intermediate part (interposed nuclei) B. Cerebellar hemisphere, lateral part (dentate nuclei) **C. Flocculonodular (lateral vestibular nucleus)** D. Vermis (fastigial nucleus) E. None of the above

Answer 93

A. Cerebellar hemisphere, intermediate part (interposed nuclei) B. Cerebellar hemisphere, lateral part (dentate nuclei) C. Flocculonodular (lateral vestibular nucleus) **D. Vermis (fastigial nucleus)** E. None of the above

Answer 94

A. Cerebellar hemisphere, intermediate part (interposed nuclei) B. Cerebellar hemisphere, lateral part (dentate nuclei) C. Flocculonodular (lateral vestibular nucleus) D. Vermis (fastigial nucleus) **E. None of the above**

Answer 95

A. Cerebellar hemisphere, intermediate part (interposed nuclei) B. Cerebellar hemisphere, lateral part (dentate nuclei) C. Flocculonodular (lateral vestibular nucleus) **D. Vermis (fastigial nucleus)** E. None of the above

Answer 96

A. Cerebellar hemisphere, intermediate part (interposed nuclei) **B. Cerebellar hemisphere, lateral part (dentate nuclei)** C. Flocculonodular (lateral vestibular nucleus) D. Vermis (fastigial nucleus) E. None of the above

Answer 97

A. Cerebellar hemisphere, intermediate part (interposed nuclei) **B. Cerebellar hemisphere, lateral part (dentate nuclei)** C. Flocculonodular (lateral vestibular nucleus) D. Vermis (fastigial nucleus) E. None of the above ## Footnote The cells of the interposed nuclei are associated with the paravermal cortex and spinocerebellum, which cont ributes to posture, muscle tone, and muscle activity of the trunk and limbs during stereotyped act ivit ies—injuries to the interposed nuclei and associated cortex (A) m ay lead to appendicular ataxia. The cells of the dentate nucleus are associated with the lateral cerebellar cortex and cerebrocerebellum, which participate in planning and coordination of skilled movement . Lesions to the dentate nucleus and associated cortex (B) can result in terminal tremor, decomposition of multijoint movements, and delay in initiating movements. Lesions to the occulonodular lobe and lateral vestibular nucleus (C) may lead to nystagmus; generally, the occulonodular lobe is involved in balance, posture, and the coordinat ion of head and neck movements via its reciprocal connections with the vestibular system. The vermis is part of the spinocerebellum and is largely responsible for the maintenance and coordination of axial and girdle musculature and the fast igial nucleus is associated with the vestibulocerebellum. Injuries to the vermis and fastigial nucleus (D) may lead to truncal ataxia, scanning speech, and hypotonia. Lesions to the cerebellum are not known to cause hypertonia (E)

Answer 98

**A. Arginine** B. Citrulline C. Lysine D. Ornithine E. Tyrosine ## Footnote Nitric oxide production in neurons is from l -arginine (A) and molecular oxygen by nit ric oxide synthetase acting in conjunction with the cofactor, reduced nicotinamide adenine dinucleotide phosphate (NADPH), and Ca21 ions. The arginine (A) is converted to citrulline (B).

Answer 99

A. Acetylcholine B. Dopamine C. Histidine D. Norepinephrine **E. Serotonin** ## Footnote The pineal gland synthesizes melatonin from serotonin (E) by the action of two enzymes sensit ive to variat ions of diurnal light. The rhythmic uctuations in melatonin synthesis are directly related to the daily light cycle.10

Answer 100

A. Muscarinic receptor B. Nicotinic receptor **C. Both** D. Neither

Answer 101

A. Muscarinic receptor **B. Nicotinic receptor** C. Both D. Neither

Answer 102

A. Muscarinic receptor B. Nicotinic receptor **C. Both** D. Neither

Answer 103

A. Muscarinic receptor **B. Nicotinic receptor** C. Both D. Neither

Answer 104

**A. Muscarinic receptor** B. Nicotinic receptor C. Both D. Neither ## Footnote The nicotinic and muscarinic receptors both (C) bind acetylcholine and are found in sympathetic neurons, whereas the directly gated receptors in skeletal muscle are nicotinic (B). Hexamethonium selectively blocks nicotinic ACh receptors (B). Muscarinic receptors (A) activate second m essenger systems via G proteins, whereas nicotinic receptors are ligand-gated ion channels.

Answer 105

A. Cl 2 ch an n els on ly B. Cl 2 an d Na 1 ch an n els C. K 1 ch an n els on ly **D. Na 1 an d K 1 channels** E. Na 1 an d Cl 2 ch an n els ## Footnote The excitatory postsynaptic potential in spinal motor neurons is mediated by the action of acetylcholine on the acetylcholine receptor (a nonselective cation channel), which increases membrane permeability to both Na1 and K1 (D)

Answer 106

A. I, II, III B. I, III C. II, IV D. IV **E. All of the above** ## Footnote Increased mean arterial pressure leads to increased stretch across the baroreceptors located in the carotid sinus (carried to the brainstem w ith the glossopharyngeal nerve) leading to re ex vasodilation and bradycardia. These e ects are mediated by decreased sympathetic tone and increased vagal tone, which leads to a decrease in heart rate and cardiac contractility, as well as systemic vasodilation, lowering systemic vascular resistance as well as blood pressure

Answer 107

A. Thick filaments **B. Thin filaments** C. Both D. Neither

Answer 108

**A. Thick filaments** B. Thin filaments C. Both D. Neither

Answer 109

A. Thick filaments **B. Thin filaments** C. Both D. Neither

Answer 110

A. Thick filaments **B. Thin filaments** C. Both D. Neither

Answer 111

**A. Thick filaments** B. Thin filaments C. Both D. Neither

Answer 112

A. Thick filaments B. Thin filaments **C. Both** D. Neither

Answer 113

A. Thick filaments **B. Thin filaments** C. Both D. Neither ## Footnote Thin laments (B) consist of actin, tropomyosin, and troponin and are at tached to the Z disks. Thick laments (A) are composed of multiple myosin molecules and bind ADP during rest. A sarcomere is the building block of a myo bril and extends from one Z disk to the next. A sarcomere is composed of both (C) thick and thin laments

Answer 114

A. Calcium binds to tropomyosin. **B. Rotation of myosin heads pulls thin laments toward the center of the sarcomere** C. The detachment of cross bridges does not require ATP. D. The dissociation of actin from myosin uses energy from the hydrolysis of GTP. E. When muscle relaxes, calcium di uses into the sarcoplasmic reticulum from the intracellular space. ## Footnote During skeletal muscle contraction, calcium binds to troponin (A is false). Both the associat ion and detachment of cross bridges require ATP (not GTP; C and D are false). During relaxation, Ca21 is actively pumped out of the intracellular space and back into the sarcoplasmic reticulum (E is false)

Answer 115

A. 2 90 mV **B. 2 65 mV** C. 2 50 mV D. 1 50 mV E. 1 65 mV ## Footnote The rest ing potential of a neuron is approximately 2 65 mV (B). The other responses are incorrect

Answer 116

**A. Alcohol** B. Angiotensin II C. Decreased blood volume D. Vomiting E. Increased plasma osmolality ## Footnote Antidiuretic hormone, or arginine vasopressin, is secreted by the posterior pituitary gland and inhibits renal excretion of free water. Increased plasma osmolality (E) stimulates osmoreceptor cells in the hypothalamus, w hich leads to the release of ADH. Volume contraction, or decreased blood volume (C), promotes ADH release via three mechanisms: (1) At a xed osmolality, volume contraction increases the rate of ADH release—during a low-volume state, a low plasma osmolality that would normally inhibit the release of ADH would allow ADH secretion to continue. (2) Low left atrial pressure decreases the ring of vagal a erents, leading to increased ADH secretion. (3) Low circulating blood volume leads to renin production by the juxtaglomerular apparatus in the kidneys. Renin is converted to angiotensin II (B), which acts on the subfornical organ and organum vasculosum of the lamina terminalis to stimulate ADH release. Pain and nausea (D) tend to promote ADH secretion. Alcohol (A) inhibits the release of ADH from the posterior pituitary gland.

Answer 117

A. A speci c mechanism exists for removing it from its site of action B. It is present in the presynaptic terminal and is released in amounts suf cient to exert its action on the postsynaptic neuron or e ector organ C. It is synthesized in the neuron **D. The enzymes that catalyze the steps in its synthesis are cytoplasmic** E. The exogenously applied substance should mimic the action of the endogenously released transmitter ## Footnote The enzymes that catalyze the synthesis of the low-molecular-weight transmit ters are usually cytoplasmic (dopamine-b-hydroxylase is an except ion), but this is not a criterion that must be ful lled for a chemical to be considered a transmit ter (D is false).

Answer 118

A. Epinephrine B. Glycine C. Histamine D. Serotonin **E. Vasoactive intestinal polypeptide (VIP)** ## Footnote VIP (E) is considered a neuroactive peptide, not a neurotransmitter. The other choices listed are considered to be neurotransmit ters: epinephrine (A), glycine (B), histamine (C), and serotonin (D).

Answer 119

A. Gastrointestinal tract B. Heart C. Lungs and bronchi D. Salivary glands **E. Sweat glands** ## Footnote In general, postganglionic sympathetic neurons release norepinephrine. Sweat glands (E) are an except ion to this rule, however. Sweat glands are innervated by sympathet ic neurons that release acetylcholine and act via muscarinic receptors. The sweat glands are innervated by the sympathetic system only

Answer 120

A. Their activation during active muscle contraction allows muscle spindles to sense changes in length **B. Their activity is increased after lesions of the spinocerebellum** C. They innervate intrafusal fibers D. Dynamic gamma motor neurons innervate dynamic nuclear bag bers only E. Static gamma motor neurons innervate nuclear chain bers and static nuclear bag bers ## Footnote Upon st imulation of extrafusal muscle bers innervated by a m otor neurons, the muscle spindles (intrafusal bers) would have a tendency to go slack, which would make them insensitive to further changes in length. g motor neurons innervate intrafusal bers (C), causing intrafusal bers to contract to sense ongoing changes in length of the muscle (A). The activit y of g m otor neurons is profoundly reduced by lesions in the cerebellum (B is false).

Answer 121

A. I, II, III B. I, III **C. II, IV** D. IV E. All of the above ## Footnote Descending serotonergic pathways (from rost roventral medullary neurons) and noradrenergic pathways (from the pons) are important links in the supraspinal modulat ion of nociceptive t ransmission

Answer 122

A. I, II, III **B. I, III** C. II, IV D. IV E. All of the above ## Footnote Cells of the retina and lateral geniculate nucleus have concentric recept ive elds that fall into two classes: on-center or o -center. Simple cells of the visual cortex have rectangular recept ive elds. The recept ive eld of a complex cell in the primary visual cortex has no clearly dist inct excitatory or inhibitory zones. Orientation but not posit ion of the light stimulus is important.

Answer 123

A. Free nerve endings B. Meissner’s corpuscles C. Merkel’s receptors D. Pacinian corpuscles **E. Ruffini’s corpuscles**

Answer 124

A. Free nerve endings **B. Meissner’s corpuscles** C. Merkel’s receptors D. Pacinian corpuscles E. Ruffini’s corpuscles

Answer 125

A. Free nerve endings B. Meissner’s corpuscles **C. Merkel’s receptors** D. Pacinian corpuscles E. Ruffini’s corpuscles

Answer 126

A. Free nerve endings B. Meissner’s corpuscles C. Merkel’s receptors **D. Pacinian corpuscles** E. Ruffini’s corpuscles

Answer 127

**A. Free nerve endings** B. Meissner’s corpuscles C. Merkel’s receptors D. Pacinian corpuscles E. Ruffini’s corpuscles ## Footnote Meissner’s corpuscles (B) and Merkel’s receptors (C) are both found super - cially in the dermal papillae and have small recept ive elds. Pacinian (D) and Ru ni’s (E) corpuscles are found in the deeper subcutaneous tissue and have large receptive elds. Both Merkel’s receptors (C) and Ru ni’s corpuscles (E) are slowly adapt ing and subserve pressure sensation. Pacinian corpuscles (D) are m ore sensitive to low- than high-frequency stimuli and transmit utter. Pain sensation is transmitted by free nerve endings (A).

Answer 128

A. Anti-amphiphysin B. Anti-gephyrin **C. Anti-glutamic acid decarboxylase** D. Anti-Yo E. Anti-Ri ## Footnote The diagnosis in the case is “sti -man” or “sti -person” syndrome. Most cases of this disorder show circulating autoantibodies against glutamic acid decarboxylase (C), which is the enzyme responsible for synthesizing GABA. The st i - person syndrome can occur rarely as a paraneoplastic syndrome in associat ion with breast cancer; in those cases, it is associated with an anti-amphiphysin (A) or an anti-gephyrin (B) autoantibody. The anti-Yo (D) antibody occurs with ovarian, lung, and Hodgkin tumors and causes cerebellar degeneration. The anti-Ri (E) antibody is responsible for the opsoclonus-myoclonus-ataxia seen with some breast and small-cell lung cancers

Answer 129

A. Bilateral vestibular schwannomas B. Gain of function mutation in a tumor promoter C. Mutation associated with chromosome 22 **D. Mutation a ecting the RAS signal-transduction pathway** E. Mutation of the hamartin gene locus on chromosome 9 ## Footnote This young pat ient presenting with an opt ic tract glioma may carry a diagnosis of neuro bromatosis type 1 (NF1). NF1 is associated with neuro bromas, optic nerve and tract gliomas, pigmented nodules of the iris, and hyperpigmented cutaneous macules. The NF1 gene is located on chromosome 17 and encodes the protein neuro bromin. Neuro bromin is thought to be a tumor suppressor gene (B is false) that has some structural homology to the RAS superfamily of GTPases. Therefore, choice D is correct. Neuro bromatosis type 2 is associated with bilateral vestibular schwannomas (A) and is caused by a mutation on chromosome 22 (C). Tuberous sclerosis is associated with mutations of the hamartin gene on chromosome 9 (E).12

Answer 130

A. G0 /G1 **B. G1 /S** C. G1 /G0 D. G2 /M E. S/G ## Footnote The G1/S transition (B) represents the point of no return in the cell cycle. At this point, DNA is checked for accuracy prior to entering the S phase. If DNA repair is not possible, apoptot ic mechanisms are activated. Another checkpoint exists at the G2/M transition (D), which is particularly important for cells exposed to ionizing radiat ion.12

Answer 131

A. MIB1 labeling index allows for the more accurate diagnosis of glioblastoma B. MIB1 labeling index does not provide any advantage over H&E staining **C. MIB1 labels cells proliferating in multiple stages of the cell cycle** D. Mitoses are more obvious with MIB1 staining E. World Health Organization (WHO) grading of brillary astrocytomas depends on MIB1 labeling index ## Footnote Traditional H&E staining techniques rely on the ident i cat ion of mitoses for the detect ion of proliferating cells. The key advantage of MIB1 labeling is the ability to detect proliferating cells in multiple stages of the cell cycle (C), even those not currently in the M phase of the cell cycle. MIB1 labeling does add data that standard techniques cannot provide, so choice B is incorrect. Mitoses are typically counted on the H&E preparat ion, and while cells undergoing mitosis are posit ive for MIB1, choice D is not the best answer. While MIB1 labeling may be useful in determining the proliferat ive index of a tumor, it is not a part of the WHO criteria for the grading of brillary astrocytomas (A and E)

Answer 132

**A. Value is higher in CSF than plasma.** B. Value is higher in plasma than CSF. C. Value is equal in plasma and CSF.

Answer 133

A. Value is higher in CSF than plasma. **B. Value is higher in plasma than CSF.** C. Value is equal in plasma and CSF.

Answer 134

**A. Value is higher in CSF than plasma.** B. Value is higher in plasma than CSF. C. Value is equal in plasma and CSF.

Answer 135

A. Value is higher in CSF than plasma. **B. Value is higher in plasma than CSF.** C. Value is equal in plasma and CSF.

Answer 136

A. Value is higher in CSF than plasma. B. Value is higher in plasma than CSF. **C. Value is equal in plasma and CSF.**

Answer 137

A. Value is higher in CSF than plasma. **B. Value is higher in plasma than CSF.** C. Value is equal in plasma and CSF.

Answer 138

A. Value is higher in CSF than plasma. B. Value is higher in plasma than CSF. **C. Value is equal in plasma and CSF.**

Answer 139

A. Value is higher in CSF than plasma. **B. Value is higher in plasma than CSF.** C. Value is equal in plasma and CSF. ## Footnote CSF contains a higher concentrat ion of chloride than the blood plasma. Beta-2 transferrin is a component that is unique to CSF and can be helpful in the diagnosis of CSF leak (A). Osmolalit y and sodium concentration are equal between CSF and plasma (C). The concentrat ions of potassium, calcium, uric acid, and glucose are lower in CSF than in plasma (B).

Answer 140

A. Caudate atrophy B. Genetic abnormality localizes to chromosome 4 **C. Increased acetylcholine transferase activity** D. Progressive choreoathetosis E. Trinucleotide CAG repeat ## Footnote Hunt ington’s disease is a fatal, autosomal dominant, progressive choreoathetosis (D) that involves a trinucleotide CAG (E) repeat on chromosome 4 (B). Brain imaging reveals atrophy of the caudate heads (A) w ith a characterist ic appearance of hydrocephalus ex vacuo. While the pathophysiology is not well understood, there is believed to be decreased acetylcholine transferase activity in pat ients with Huntington’s disease (C is false).

Answer 141

A. 2 94 mV B. 2 90 mV C. 2 86 mV **D. 1 61 mV** E. 1 267 mV ## Footnote The equilibrium potential is the membrane potential at which no net di usion of an ion occurs because of balanced elect rical and chemical gradients. The resting membrane potent ial for sodium is 1 61 mV (D), potassium is 2 94 mV (A), chloride is 2 86 mV (C), and calcium is 1 267 mV (E). The rest ing membrane potential of large, myelinated peripheral nerves is approximately 2 90 mV (B). The resting membrane potential is determined largely by the equilibrium potent ial of potassium (2 94 mV) because potassium is 100 times more permeable than sodium.

Answer 142

**A. Methylation of the MGMT gene’s prom oter region upregulates MGMT gene expression** B. MGMT m ethylation predicts im proved sur vival C. MGMT m ethylation predicts im proved ben e t from tem ozolom ide D. The MGMT gen e en codes a DNA repair protein E. The MGMT gen e prom otes ch em oth erapy resistan ce ## Footnote The O6-methylguanine-DNA methyltransferase (MGMT) gene codes for a DNA repair protein (D) that represents an important mechanism for chemotherapy resistance (E) in glioblastoma. Methylation of the gene’s promoter region leads to silencing of the MGMT gene (A is false). MGMT m ethylation is an independent predictor of improved survival (B) as well as a predictor of survival bene t from temozolomide (C) in pat ients with glioblastoma

Answer 143

**A. 4 minutes** B. 15 minutes C. 40 minutes D. 80 minutes E. Infnite

Answer 144

A. 4 minutes B. 15 minutes **C. 40 minutes** D. 80 minutes E. Infnite

Answer 145

A. 4 minutes B. 15 minutes C. 40 minutes **D. 80 minutes** E. Infnite

Answer 146

A. 4 minutes B. 15 minutes C. 40 minutes D. 80 minutes **E. Infnite**

Answer 147

A. 4 minutes B. 15 minutes C. 40 minutes D. 80 minutes **E. Infnite** ## Footnote Normal cerebral blood ow (CBF) is 50–55 mL/100 g/min (E). Cells can compensate at a CBF of 18 mL/100 g/min indefinitely (E). CBF in the ischemic penumbra is thought to be 8–23 mL/100 g/min. At less than 8 mL/100 g/min, there is rapid cell death from ion pump failure (A). At 10 mL/100 g/min, cell death occurs after approximately 40 minutes (C). At 15 mL/100 g/min cell death occurs after 80 minute (D).

Answer 148

A. Anti-glutamic acid decarboxylase B. Anti-Hu **C. Anti-Ma** D. Anti-Ri E. Anti-Yo

Answer 149

A. Anti-glutamic acid decarboxylase B. Anti-Hu C. Anti-Ma D. Anti-Ri **E. Anti-Yo**

Answer 150

A. Anti-glutamic acid decarboxylase **B. Anti-Hu** C. Anti-Ma D. Anti-Ri E. Anti-Yo

Answer 151

A. Anti-glutamic acid decarboxylase B. Anti-Hu C. Anti-Ma **D. Anti-Ri** E. Anti-Yo

Answer 152

**A. Anti-glutamic acid decarboxylase** B. Anti-Hu C. Anti-Ma D. Anti-Ri E. Anti-Yo ## Footnote Limbic encephalitis is a subacute encephalitis that t ypically involves the mesial temporal lobes, cingulate gyri, and insula. Limbic encephalitis is associated with testicular cancer, lung cancer, and anti-Ma (C) antibodies. Anti-Yo (E) ant ibodies are associated with ovarian and breast cancer and lead to cerebellar degenerat ion. Anti-Hu (B) ant ibodies are associated w ith oat cell pulmonary carcinoma and lymphoma and are associated with sensory neuropathy, encephalit is, and cerebellar degenerat ion. Anti-Ri (D) antibodies are associated with breast cancer and lead to opsoclonus. Sti -man syndrome is associated with antibodies to glutamic acid decarboxylase (A) in . 60% of cases.