Neurobiology Flashcards
A strong mitogen
A. Bone growth factors
B. Recombinant human bone morphogenic proteins
C. Both
D. Neither
A. Bone growth factors
B. Recombinant human bone morphogenic proteins
C. Both
D. Neither
Bo n e g ro w th facto rs (A) are strong m itogens and act on di erentiated m esenchymal cells of the chondro-osseous lineage. Re c o m b i n a n t h u m a n b o n e morphogenic proteins (B) are potent inducers of bone cell di erentiation and may act on undi erentiated mesenchymal cells. Both bone growth factors (A) and bone morphogenic proteins (B) are polypeptides. 1
A potent inducer of bone cell di erentiation
A. Bone growth factors
B. Recombinant human bone morphogenic proteins
C. Both
D. Neither
A. Bone growth factors
B. Recombinant human bone morphogenic proteins
C. Both
D. Neither
Bo n e g ro w th facto rs (A) are strong m itogens and act on di erentiated m esenchymal cells of the chondro-osseous lineage. Re c o m b i n a n t h u m a n b o n e morphogenic proteins (B) are potent inducers of bone cell di erentiation and may act on undi erentiated mesenchymal cells. Both bone growth factors (A) and bone morphogenic proteins (B) are polypeptides. 1
Act on di erentiated mesenchymal cells of the chondro-osseous lineage
A. Bone growth factors
B. Recombinant human bone morphogenic proteins
C. Both
D. Neither
A. Bone growth factors
B. Recombinant human bone morphogenic proteins
C. Both
D. Neither
Bo n e g ro w th facto rs (A) are strong m itogens and act on di erentiated m esenchymal cells of the chondro-osseous lineage. Re c o m b i n a n t h u m a n b o n e morphogenic proteins (B) are potent inducers of bone cell di erentiation and may act on undi erentiated mesenchymal cells. Both bone growth factors (A) and bone morphogenic proteins (B) are polypeptides. 1
Act on undi erentiated mesenchymal cells
A. Bone growth factors
B. Recombinant human bone morphogenic proteins
C. Both
D. Neither
A. Bone growth factors
B. Recombinant human bone morphogenic proteins
C. Both
D. Neither
Bo n e g ro w th facto rs (A) are strong m itogens and act on di erentiated m esenchymal cells of the chondro-osseous lineage. Re c o m b i n a n t h u m a n b o n e morphogenic proteins (B) are potent inducers of bone cell di erentiation and may act on undi erentiated mesenchymal cells. Both bone growth factors (A) and bone morphogenic proteins (B) are polypeptides. 1
Polypeptides
A. Bone growth factors
B. Recombinant human bone morphogenic proteins
C. Both
D. Neither
A. Bone growth factors
B. Recombinant human bone morphogenic proteins
C. Both
D. Neither
Bo n e g ro w th facto rs (A) are strong m itogens and act on di erentiated m esenchymal cells of the chondro-osseous lineage. Re c o m b i n a n t h u m a n b o n e morphogenic proteins (B) are potent inducers of bone cell di erentiation and may act on undi erentiated mesenchymal cells. Both bone growth factors (A) and bone morphogenic proteins (B) are polypeptides. 1
Which of the following is the correct representation of the subunits of the acetylcholine (ACh) receptor at the neurom uscular junction?
A. abgd
B. a 2bgd
C. ab2gd
D. abg2d
E. abgd2
A. abgd
B. a 2bgd
C. ab2gd
D. abg2d
E. abgd2
Ace t y lch o lin e r e ce p t o r s c a n b e d iv id e d in t o m u s c a r in ic a n d n ico t in ic t y p e s . Th e m u scar in ic acet ylch olin e re ce p t or s a re p r ese n t in all p ost ga n glion ic p a r asympathetic terminals and in the postganglionic sympathetic terminals innervating sweat glands. The muscarinic acetylcholine receptor is a G-proteincoupled receptor and therefore transm its its signals via a second m essenger system. Nicotinic acetylcholine receptors function as cation-selective ion channels. Nicotinic acetylcholine receptors are present at the neurom uscular junction and at the preganglionic term inals of sympathetic and parasympathetic bers. Autonomic nicotinic acetylcholine receptors consist of a and b subunits only, i.e., a 2b 2 or a 3b 3. How ever, t h e n icot in ic acet ylch olin e recep tor at the neuromuscular junction is a pentamer consisting of two a , on e b, one γ, and one δ subunit, i.e., a 2bgd (B)
Which of the following is true of the a subunit of the nicotinic acetylcholine receptor?
A. It contains four hydrophobic transmembrane portions.
B. The binding site is not located on the a subun it .
C. The cytoplasmic loop is the most highly conserved portion of the subunit.
D. The N terminal is extracellular, and the C terminal is intracellular.
E. The transmembrane portion is the least conserved segment.
A. It contains four hydrophobic transmembrane portions.
B. The binding site is not located on the a subun it .
C. The cytoplasmic loop is the most highly conserved portion of the subunit.
D. The N terminal is extracellular, and the C terminal is intracellular.
E. The transmembrane portion is the least conserved segment.
Th e liga n d b in d in g sit e is locat e d on t h e a su bu n it (B is false), t h e t ran sm em brane segment is the most highly conserved (E is false), an d th e cytop lasm ic loop connecting M3 and M4 is the least highly conserved (C is false). Both t h e N and the C term inals are extracellular (D is false). Resp on se A is correct . 2,5
The number of binding sites on the nicotinic acetylcholine receptor is
A. 1
B. 2
C. 3
D. 4
E. 5
A. 1
B. 2
C. 3
D. 4
E. 5
Each n icot in ic a cet ylch olin e re ce p t or com p lex h a s two extracellular acetylcholine binding sites (B) that are primarily composed of six amino acids located on the a subunits. 2,6
Binds g-aminobutyric acid (GABA)
A. a subun it of GABAA
receptor
B. b su bun it of GABAA
receptor
C. Both
D. Neither
A. a subun it of GABAA
receptor
B. b su bun it of GABAA
receptor
C. Both
D. Neither
Th e GABAA receptor functions as a chloride ion channel and is activated by multiple ligands including benzodiazepines, barbiturates, and zolpidem. The binding site for GABA on the GABAA receptor is located between the a and b subunits (C). Th e bin d ing site for ben zod iazep in es is located bet w een th e a and gamma subunits (A). 4
Binds benzodiazepines
A. a subun it of GABAA
receptor
B. b su bun it of GABAA
receptor
C. Both
D. Neither
A. a subun it of GABAA
receptor
B. b su bun it of GABAA
receptor
C. Both
D. Neither
Th e GABAA receptor functions as a chloride ion channel and is activated by multiple ligands including benzodiazepines, barbiturates, and zolpidem. The binding site for GABA on the GABAA receptor is located between the a and b subunits (C). Th e bin d ing site for ben zod iazep in es is located bet w een th e a and gamma subunits (A). 4
Most closely linked with synaptic plasticity and cell death
A. GABA receptor
B. Glutamate receptor
C. Glycine receptor
D. Nicotinic ACh receptor
E. Serotonin (5-HT) receptor
A. GABA receptor
B. Glutamate receptor
C. Glycine receptor
D. Nicotinic ACh receptor
E. Serotonin (5-HT) receptor
GABA re c e p t o r s (A) have been characterized as the site of action of benzodiazepines. Ligand-gated glutamate receptors (B) can be divided into NMDA and non-NMDA receptors. The N-methyl-d -aspartate (NMDA) receptor is voltage regulated in that the open channel is occluded at norm al resting potential by Mg 21 . Dep olarizat ion d rives Mg 21 ou t of t h e cell, a llow in g ot h e r ion s to pass. High concentrations of glutamate may induce neuronal cell death via activation of NMDA and AMPA (a non-NMDA glutamate receptor [B]), allowing calcium in ux into the cell. Glycine receptors share many features of the GABAA receptor. Both function as ligand-gated chloride ion channels and are present throughout the brainstem and spinal cord. The glycine receptor (C) is a n t agon ize d by st r ych n in e . Nicot in ic a cet ylch o lin e re ce p t or s fu n ct io n a s cation-selective ion channels. Nicotinic acetylcholine receptors (D) a r e p r e sent at the neuromuscular junction and at the preganglionic terminals of sympathetic and parasympathetic bers. Se ro to n in re ce pto rs (E) can be fou n d at multiple sites and are prominent in the dorsal raphe nucleus. 5
GABA and this receptor are permeable to chloride ions
A. GABA receptor
B. Glutamate receptor
C. Glycine receptor
D. Nicotinic ACh receptor
E. Serotonin (5-HT) receptor
A. GABA receptor
B. Glutamate receptor
C. Glycine receptor
D. Nicotinic ACh receptor
E. Serotonin (5-HT) receptor
GABA re c e p t o r s (A) have been characterized as the site of action of benzodiazepines. Ligand-gated glutamate receptors (B) can be divided into NMDA and non-NMDA receptors. The N-methyl-d -aspartate (NMDA) receptor is voltage regulated in that the open channel is occluded at norm al resting potential by Mg 21 . Dep olarizat ion d rives Mg 21 ou t of t h e cell, a llow in g ot h e r ion s to pass. High concentrations of glutamate may induce neuronal cell death via activation of NMDA and AMPA (a non-NMDA glutamate receptor [B]), allowing calcium in ux into the cell. Glycine receptors share many features of the GABAA receptor. Both function as ligand-gated chloride ion channels and are present throughout the brainstem and spinal cord. The glycine receptor (C) is a n t agon ize d by st r ych n in e . Nicot in ic a cet ylch o lin e re ce p t or s fu n ct io n a s cation-selective ion channels. Nicotinic acetylcholine receptors (D) a r e p r e sent at the neuromuscular junction and at the preganglionic terminals of sympathetic and parasympathetic bers. Se ro to n in re ce pto rs (E) can be fou n d at multiple sites and are prominent in the dorsal raphe nucleus. 5
Binds strychnine
A. GABA receptor
B. Glutamate receptor
C. Glycine receptor
D. Nicotinic ACh receptor
E. Serotonin (5-HT) receptor
A. GABA receptor
B. Glutamate receptor
C. Glycine receptor
D. Nicotinic ACh receptor
E. Serotonin (5-HT) receptor
GABA re c e p t o r s (A) have been characterized as the site of action of benzodiazepines. Ligand-gated glutamate receptors (B) can be divided into NMDA and non-NMDA receptors. The N-methyl-d -aspartate (NMDA) receptor is voltage regulated in that the open channel is occluded at norm al resting potential by Mg 21 . Dep olarizat ion d rives Mg 21 ou t of t h e cell, a llow in g ot h e r ion s to pass. High concentrations of glutamate may induce neuronal cell death via activation of NMDA and AMPA (a non-NMDA glutamate receptor [B]), allowing calcium in ux into the cell. Glycine receptors share many features of the GABAA receptor. Both function as ligand-gated chloride ion channels and are present throughout the brainstem and spinal cord. The glycine receptor (C) is a n t agon ize d by st r ych n in e . Nicot in ic a cet ylch o lin e re ce p t or s fu n ct io n a s cation-selective ion channels. Nicotinic acetylcholine receptors (D) a r e p r e sent at the neuromuscular junction and at the preganglionic terminals of sympathetic and parasympathetic bers. Se ro to n in re ce pto rs (E) can be fou n d at multiple sites and are prominent in the dorsal raphe nucleus. 5
Binds benzodiazepine
A. GABA receptor
B. Glutamate receptor
C. Glycine receptor
D. Nicotinic ACh receptor
E. Serotonin (5-HT) receptor
A. GABA receptor
B. Glutamate receptor
C. Glycine receptor
D. Nicotinic ACh receptor
E. Serotonin (5-HT) receptor
GABA re c e p t o r s (A) have been characterized as the site of action of benzodiazepines. Ligand-gated glutamate receptors (B) can be divided into NMDA and non-NMDA receptors. The N-methyl-d -aspartate (NMDA) receptor is voltage regulated in that the open channel is occluded at norm al resting potential by Mg 21 . Dep olarizat ion d rives Mg 21 ou t of t h e cell, a llow in g ot h e r ion s to pass. High concentrations of glutamate may induce neuronal cell death via activation of NMDA and AMPA (a non-NMDA glutamate receptor [B]), allowing calcium in ux into the cell. Glycine receptors share many features of the GABAA receptor. Both function as ligand-gated chloride ion channels and are present throughout the brainstem and spinal cord. The glycine receptor (C) is a n t agon ize d by st r ych n in e . Nicot in ic a cet ylch o lin e re ce p t or s fu n ct io n a s cation-selective ion channels. Nicotinic acetylcholine receptors (D) a r e p r e sent at the neuromuscular junction and at the preganglionic terminals of sympathetic and parasympathetic bers. Se ro to n in re ce pto rs (E) can be fou n d at multiple sites and are prominent in the dorsal raphe nucleus. 5
One type of this receptor is both ligand and voltage regulated
A. GABA receptor
B. Glutamate receptor
C. Glycine receptor
D. Nicotinic ACh receptor
E. Serotonin (5-HT) receptor
A. GABA receptor
B. Glutamate receptor
C. Glycine receptor
D. Nicotinic ACh receptor
E. Serotonin (5-HT) receptor
GABA re c e p t o r s (A) have been characterized as the site of action of benzodiazepines. Ligand-gated glutamate receptors (B) can be divided into NMDA and non-NMDA receptors. The N-methyl-d -aspartate (NMDA) receptor is voltage regulated in that the open channel is occluded at norm al resting potential by Mg 21 . Dep olarizat ion d rives Mg 21 ou t of t h e cell, a llow in g ot h e r ion s to pass. High concentrations of glutamate may induce neuronal cell death via activation of NMDA and AMPA (a non-NMDA glutamate receptor [B]), allowing calcium in ux into the cell. Glycine receptors share many features of the GABAA receptor. Both function as ligand-gated chloride ion channels and are present throughout the brainstem and spinal cord. The glycine receptor (C) is a n t agon ize d by st r ych n in e . Nicot in ic a cet ylch o lin e re ce p t or s fu n ct io n a s cation-selective ion channels. Nicotinic acetylcholine receptors (D) a r e p r e sent at the neuromuscular junction and at the preganglionic terminals of sympathetic and parasympathetic bers. Se ro to n in re ce pto rs (E) can be fou n d at multiple sites and are prominent in the dorsal raphe nucleus. 5
One type of this receptor is blocked by magnesium ions
A. GABA receptor
B. Glutamate receptor
C. Glycine receptor
D. Nicotinic ACh receptor
E. Serotonin (5-HT) receptor
A. GABA receptor
B. Glutamate receptor
C. Glycine receptor
D. Nicotinic ACh receptor
E. Serotonin (5-HT) receptor
GABA re c e p t o r s (A) have been characterized as the site of action of benzodiazepines. Ligand-gated glutamate receptors (B) can be divided into NMDA and non-NMDA receptors. The N-methyl-d -aspartate (NMDA) receptor is voltage regulated in that the open channel is occluded at norm al resting potential by Mg 21 . Dep olarizat ion d rives Mg 21 ou t of t h e cell, a llow in g ot h e r ion s to pass. High concentrations of glutamate may induce neuronal cell death via activation of NMDA and AMPA (a non-NMDA glutamate receptor [B]), allowing calcium in ux into the cell. Glycine receptors share many features of the GABAA receptor. Both function as ligand-gated chloride ion channels and are present throughout the brainstem and spinal cord. The glycine receptor (C) is a n t agon ize d by st r ych n in e . Nicot in ic a cet ylch o lin e re ce p t or s fu n ct io n a s cation-selective ion channels. Nicotinic acetylcholine receptors (D) a r e p r e sent at the neuromuscular junction and at the preganglionic terminals of sympathetic and parasympathetic bers. Se ro to n in re ce pto rs (E) can be fou n d at multiple sites and are prominent in the dorsal raphe nucleus. 5
Signi cantly permeable to calcium ions
A. Kainate receptor only
B. N-methyl-d -aspartate (NMDA) receptor only
C. Quisqualate/a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid
(AMPA) receptor on ly
D. A an d B
E. A, B, an d C
A. Kainate receptor only
B. N-methyl-d -aspartate (NMDA) receptor only
C. Quisqualate/a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid
(AMPA) receptor on ly
D. A an d B
E. A, B, an d C
Th e ligan d - gat e d glu t a m at e re ce p t or s ca n b e grou p e d in t o N-methyl-d aspartate (NMDA) receptors (B) and non-NMDA receptors, all of which increase cation conductance when activated. The non-NMDA receptors include the a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptor (C) an d t h e kainic acid (A) receptor. Th e NMDA receptor (B) can be blocked by magnesium at resting membrane potentials and is therefore both ligand and voltage gated. NMDA receptors (B) are particularly permeable to calcium ions, participate in long-term potentiation, and are thought to be im portant for neuronal plasticity, learning, and memory.
Permeable to monovalent cations
A. Kainate receptor only
B. N-methyl-d -aspartate (NMDA) receptor only
C. Quisqualate/a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid
(AMPA) receptor on ly
D. A an d B
E. A, B, an d C
A. Kainate receptor only
B. N-methyl-d -aspartate (NMDA) receptor only
C. Quisqualate/a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid
(AMPA) receptor on ly
D. A an d B
E. A, B, an d C
Th e ligan d - gat e d glu t a m at e re ce p t or s ca n b e grou p e d in t o N-methyl-d aspartate (NMDA) receptors (B) and non-NMDA receptors, all of which increase cation conductance when activated. The non-NMDA receptors include the a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptor (C) an d t h e kainic acid (A) receptor. Th e NMDA receptor (B) can be blocked by magnesium at resting membrane potentials and is therefore both ligand and voltage gated. NMDA receptors (B) are particularly permeable to calcium ions, participate in long-term potentiation, and are thought to be im portant for neuronal plasticity, learning, and memory.
Ligand-gated
A. Kainate receptor only
B. N-methyl-d -aspartate (NMDA) receptor only
C. Quisqualate/a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid
(AMPA) receptor on ly
D. A an d B
E. A, B, an d C
A. Kainate receptor only
B. N-methyl-d -aspartate (NMDA) receptor only
C. Quisqualate/a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid
(AMPA) receptor on ly
D. A an d B
E. A, B, an d C
Th e ligan d - gat e d glu t a m at e re ce p t or s ca n b e grou p e d in t o N-methyl-d aspartate (NMDA) receptors (B) and non-NMDA receptors, all of which increase cation conductance when activated. The non-NMDA receptors include the a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptor (C) an d t h e kainic acid (A) receptor. Th e NMDA receptor (B) can be blocked by magnesium at resting membrane potentials and is therefore both ligand and voltage gated. NMDA receptors (B) are particularly permeable to calcium ions, participate in long-term potentiation, and are thought to be im portant for neuronal plasticity, learning, and memory.
Voltage-gated
A. Kainate receptor only
B. N-methyl-d -aspartate (NMDA) receptor only
C. Quisqualate/a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid
(AMPA) receptor on ly
D. A an d B
E. A, B, an d C
A. Kainate receptor only
B. N-methyl-d -aspartate (NMDA) receptor only
C. Quisqualate/a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid
(AMPA) receptor on ly
D. A an d B
E. A, B, an d C
Th e ligan d - gat e d glu t a m at e re ce p t or s ca n b e grou p e d in t o N-methyl-d aspartate (NMDA) receptors (B) and non-NMDA receptors, all of which increase cation conductance when activated. The non-NMDA receptors include the a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptor (C) an d t h e kainic acid (A) receptor. Th e NMDA receptor (B) can be blocked by magnesium at resting membrane potentials and is therefore both ligand and voltage gated. NMDA receptors (B) are particularly permeable to calcium ions, participate in long-term potentiation, and are thought to be im portant for neuronal plasticity, learning, and memory.
Blocked by magnesium ions
A. Kainate receptor only
B. N-methyl-d -aspartate (NMDA) receptor only
C. Quisqualate/a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid
(AMPA) receptor on ly
D. A an d B
E. A, B, an d C
A. Kainate receptor only
B. N-methyl-d -aspartate (NMDA) receptor only
C. Quisqualate/a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid
(AMPA) receptor on ly
D. A an d B
E. A, B, an d C
Th e ligan d - gat e d glu t a m at e re ce p t or s ca n b e grou p e d in t o N-methyl-d aspartate (NMDA) receptors (B) and non-NMDA receptors, all of which increase cation conductance when activated. The non-NMDA receptors include the a -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptor (C) an d t h e kainic acid (A) receptor. Th e NMDA receptor (B) can be blocked by magnesium at resting membrane potentials and is therefore both ligand and voltage gated. NMDA receptors (B) are particularly permeable to calcium ions, participate in long-term potentiation, and are thought to be im portant for neuronal plasticity, learning, and memory.
Which of the following is true of acetylcholine (ACh) release from the neuromuscular junction?
A. One molecule of ACh equals 10,000 quanta
B. One quanta contains 10,000 molecules of ACh
C. One quanta equals 1 molecule of ACh
D. One vesicle contains 10,000 quanta
E. One vesicle contains 10 molecules
A. One molecule of ACh equals 10,000 quanta
B. One quanta contains 10,000 molecules of ACh
C. One quanta equals 1 molecule of ACh
D. One vesicle contains 10,000 quanta
E. One vesicle contains 10 molecules
Qu an t a refers to th e acet ych olin e qu an t it y of on e syn apt ic vesicle an d h as been estimated in the range of 1,000 to 50,000 molecules of Ach per vesicle (per quanta). 5
Pro-opiomelanocortin is a precursor of
I. Ad ren ocor t icot rop ic h or m on e (ACTH)
II. a -melanocyte-stimulating hormone (MSH)
III. b -endorphin
IV. b -lipotropin
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
Pre-proopiom elanocortin (POMC) is an opioid precursor peptide along w ith pre-proenkephalin and pre-prodynorphin. The major opioid peptide derived from POMC is b -endorphin. POMC is also conver ted in to t h e n on op ioid peptides adrenocorticotropic hormone (ACTH), melanocyte-stimulating hormone (a -MSH), an d b -lipotropin
Removal of calcium ions from the cytosol in a presynaptic nerve terminal
follow in g an act ion p oten t ial is t h ough t to occu r by
I. Act ive t ran sp or t
II. Bin d in g to cytosolic p rotein s
III. Tran sp or t in to in t racellu lar calciu m storage vesicles
IV. Reversal of ow th rough voltage-gated calcium ch an n els
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
Re m o va l o f c a lc iu m io n s fr o m t h e c y t o s o l in a p r e s y n a p t ic n e r ve t e r m in a l follow in g an act ion p oten t ial is t h ough t to occu r by active transport, binding to cytosolic proteins, and transport into intracellular calcium storage vesicles. Reversal of ow t h rough volt age-gated ch an n els is n ot a m ech an ism of removal of Ca 21 from the cytosol. 5
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.
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.
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
Each of the following is true of G proteins except
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.
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.
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
D1 receptors act by this second messenger
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
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
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
Increased by nitric oxide
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
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
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
Generated by the action of phospholipase C
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
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
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
synergistically activates protein kinase C with calcium
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
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
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
Binds to calmodulin
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
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
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
Photoreception utilizes this second messenger
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
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
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
Opens a calcium channel in the endoplasmic reticulum, releasing free calcium into the cytosol
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
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
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
Each of the following is true of the Na 1 /K 1 pum p except th at it
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
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
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
Each of the following is true of events occurring during the action potential except
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.
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.
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
The velocity of an action potential increases with a
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
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
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
Which of the following is true of myelination?
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.
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.
Myelination increases transm em brane resistance and decreases m em brane capacitance, leading to increased conduction velocities. 6
Usually depolarizes muscle cells past threshold
A. End-plate potential
B. Miniature end-plate potential
C. Both
D. Neither
A. End-plate potential
B. Miniature end-plate potential
C. Both
D. Neither
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
Occurs in unstimulated cells
A. End-plate potential
B. Miniature end-plate potential
C. Both
D. Neither
A. End-plate potential
B. Miniature end-plate potential
C. Both
D. Neither
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
Produces a miniature action potential
A. End-plate potential
B. Miniature end-plate potential
C. Both
D. Neither
A. End-plate potential
B. Miniature end-plate potential
C. Both
D. Neither
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
Inhibitory postsynaptic potentials are produced when a transmitter opens channels permeable to
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
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
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
Which of the following is true of axonal transport?
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.
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.
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
Discharge increases with passive stretch
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
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
Discharge increases with active contraction
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
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
In series with extrafusal bers
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
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
In parallel with extrafusal bers
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
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
Sensitive to muscle tension
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
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
Sensitive to muscle length and velocity of length change
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
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
Innervated by group I (large myelinated) fibers
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
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
Innervated by group II (small myelinated) bers
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
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
Conduction velocity of a erent bers is . 120 m /s.
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
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
Contains dynamic nuclear bag, static nuclear bag, and nuclear chain bers
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
A. Golgi tendon organ
B. Muscle spindle
C. Both
D. Neither
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
Each of the following is true of decerebrate rigidity except
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.
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.
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
An antidromic wave in motor bers traveling to anterior horn cells
A. Clasp-knife response
B. Flexion reflex
C. F response
D. H response
E. M response
F. Stretch reflex
A. Clasp-knife response
B. Flexion reflex
C. F response
D. H response
E. M response
F. Stretch reflex
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
Has phasic and tonic components
A. Clasp-knife response
B. Flexion reflex
C. F response
D. H response
E. M response
F. Stretch reflex
A. Clasp-knife response
B. Flexion re ex
C. F response
D. H response
E. M response
F. Stretch reflex
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
A protective re ex involving polysynaptic reflex pathways
A. Clasp-knife response
B. Flexion reflex
C. F response
D. H response
E. M response
F. Stretch reflex
A. Clasp-knife response
B. Flexion re ex
C. F response
D. H response
E. M response
F. Stretch reflex
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
The electrical equivalent of the tendon reflex
A. Clasp-knife response
B. Flexion reflex
C. F response
D. H response
E. M response
F. Stretch reflex
A. Clasp-knife response
B. Flexion re ex
C. F response
D. H response
E. M response
F. Stretch reflex
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
The direct motor response obtained by stimulating a mixed motor sensory nerve
A. Clasp-knife response
B. Flexion reflex
C. F response
D. H response
E. M response
F. Stretch reflex
A. Clasp-knife response
B. Flexion re ex
C. F response
D. H response
E. M response
F. Stretch reflex
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
A length-dependent change in muscle force when the limb is passively moved
A. Clasp-knife response
B. Flexion reflex
C. F response
D. H response
E. M response
F. Stretch reflex
A. Clasp-knife response
B. Flexion re ex
C. F response
D. H response
E. M response
F. Stretch reflex
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
ontraction of the detrusor muscle of the bladder is achieved through activation of
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
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
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
Which is true of events occurring after a typical axon is severed?
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.
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.
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
Agents that increase the formation of cerebrospinal uid (CSF) include
I. Carbon d ioxid e
II. Norep in ep h r in e
III. Volat ile an est h et ic agen t s
IV. Carbon ic an hydrase in h ibitors
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
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
The main neurotransmitter of the Renshaw cell is thought to be
A. Acetylcholine
B. GABA
C. Glutamate
D. Glycine
E. Histamine
A. Acetylcholine
B. GABA
C. Glutamate
D. Glycine
E. Histamine
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
Auditory nerve
A. Wave I
B. Wave II
C. Wave III
D. Wave IV
E. Wave V
A. Wave I
B. Wave II
C. Wave III
D. Wave IV
E. Wave V
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
Cochlear nuclei
A. Wave I
B. Wave II
C. Wave III
D. Wave IV
E. Wave V
A. Wave I
B. Wave II
C. Wave III
D. Wave IV
E. Wave V
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
Inferior colliculus
A. Wave I
B. Wave II
C. Wave III
D. Wave IV
E. Wave V
A. Wave I
B. Wave II
C. Wave III
D. Wave IV
E. Wave V
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
Lateral lemniscus
A. Wave I
B. Wave II
C. Wave III
D. Wave IV
E. Wave V
A. Wave I
B. Wave II
C. Wave III
D. Wave IV
E. Wave V
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
Superior olivary nucleus
A. Wave I
B. Wave II
C. Wave III
D. Wave IV
E. Wave V
A. Wave I
B. Wave II
C. Wave III
D. Wave IV
E. Wave V
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
Absence or delay implies cervical cord disease
A. Erb’s point
B. N11
C. N13/P13
D. N19
E. P22
A. Erb’s point
B. N11
C. N13/P13
D. N19
E. P22
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
Absence or delay implies peripheral nerve disease
A. Erb’s point
B. N11
C. N13/P13
D. N19
E. P22
A. Erb’s point
B. N11
C. N13/P13
D. N19
E. P22
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
