Neurophysiology

Question 1

Which one of the following is NOT a component of the blood-brain barrier?
a. Capillary endothelial cells
b. Astrocytic foot processes
c. Basement membrane
d. Tight junctions
e. Microglia

Answer 1

e. Microglia

Question 2

Which one of the following statements regarding the area postrema is LEAST accurate?
a. It is located in the dorsomedial medulla in the caudal part of the fourth ventricle
b. Its blood supply is mostly from the anterior inferior cerebellar artery
c. It is a circumventricular organ
d. It plays a role as a chemoreceptor
trigger zone
e. It expresses 5-HT3 receptors

Answer 2

a. It is located in the ventral medulla at a position that is caudal to the fourth ventricle

(ini jawaban (ventral) beda dengan pilihan jawaban di soal (dorsal). Kalau ikut sesuai soal maka yg least accurate adalah (b) AICA, seharusnya PICA)

The area postrema is found in the dorsomedial medulla oblongata and can be observed as two con- vex prominences bulging into the most caudal part of the fourth ventricle. It is a V-shaped structure diverging from an apex at the obex, and receives blood supply from pyramidal branches of the posterior inferior cerebellar arteries which run along its lateral edge. It is thought to be a chemoreceptor trigger zone for vomiting and inhibition of 5-HT3 receptors here (as well as peripherally on vagal afferents) is effective in reducing the nausea associ- ated with cancer chemotherapy.

Question 3

Which one of the following statements
regarding the production of CSF by choroid
plexus cells is LEAST accurate?
a. Requires ultrafiltration of plasma to form
extracellular fluid at basolateral
membrane
b. Formation is primarily generated by net
secretion of Na+, Cl-, and HCO3- into ventricles
c. Water is actively pumped into the ventricles via Aquaporin 1 channels in the apical membrane
d. Active transport of Na+ into the ventricles
via Na+ /K+ ATPase occurs at the basolateral membrane
e. Basolateral membrane Na influx via Na+/H+ exchange and Na+/HCO3- cotransport channels.

Answer 3

c. Water is actively pumped into the ventricles via Aquaporin 1 channels in the apical membrane

CSF forms in two sequential stages. First, ultrafil- tration of plasma occurs across the fenestrated capillary wall into the ECF beneath the basolat- eral membrane of the choroid epithelial cell. Sec- ond, choroid epithelial cells secrete fluid into the ventricle. Fluid secretion into the ventricles is mediated by an array of ion transporters unevenly positioned at the blood-facing (basolateral) or CSF-facing (apical) membranes. Many ionic spe- cies are involved in CSF production (e.g., K+, Mg2+, and Ca2+). However, fluid formation is pri- marily generated by net secretion of Na+, Cl, and HCO3 into ventricles as water molecules follow them passively down a chemical gradient via Aquaporin1 channels in the apical membrane. Na+ transport into CSF occurs due to active transport via Na+/K+ ATPase exchange pump at the apical membrane, and is replaced by basolat- eral membrane Na influx via Na+/H+ exchange and Na+/HCO3 cotransport channels. Trans- port of Cl into CSF occurs via passive diffusion via apical Cl selective channels (and possibly Na+/K+/Cl cotransport), and is replaced at the basolateral membrane in exchange for HCO3. Intracellular HCO3 is accumulated by (i) hydra- tion of CO2 catalyzed by carbonic anhydrase and (ii) influx via basolateral membrane Na/HCO3 cotransport, then can enter the CSF at the apical membrane either by anion channel or Na/HCO3 cotransport. CSF has lower concentrations of K+ and amino acids than plasma does, and it contains almost no protein.

Question 4

Which one of the following statements regarding axonal transport is LEAST accurate?
a. Large membranous organelles are transported by fast kinesin dependent anterograde transport and dynein dependent
retrograde transport
b. Cytosolic proteins are transported by fast
transport
c. Occurs by retrograde transport
d. Anterograde transport is dependent upon
microtubules and the ATPase kinesin
e. Rabies virus spreads by retrograde axonal
transport

Answer 4

b. Cytosolic proteins are transported by fast
transport

Nerve cells have an elaborate transport system that moves organelles and macromolecules between the cell body and the axon and its terminals. Axonal transport from the cell body toward the terminals is called anterograde; transport from the terminals toward the cell body is called retrograde. Antero- grade axonal transport is classified into fast and slow components. Fast transport, at speeds of up to 400 mm/day, is based on the action of an ATPase protein called kinesin which moves macromolecule-containing vesicles and mitochon- dria along microtubules. Slow transport carries important structural and metabolic components from the cell body to axon terminals (e.g., cytoskel- etal protein components such as actin, myosin, tubulin, and cytosolic enzymes required for neuro- transmitter synthesis in the presynaptic terminal) but the mechanism is less clear. Retrograde axonal transport along axonal microtubules is driven by the protein dynein and allows the neuron/cell body to respond to molecules taken up near the axon ter- minal by either pinocytosis or receptor-mediated endocytosis (e.g., growth factors). In addition, this form of transport functions in the continual recy- cling of components of the axon terminal (e.g., mitochondria). Retrograde transport of rabies virus allows replication in the cell body and spread to
adjacent neurons.

Question 5

Which one of the following statements regarding the concentration of ions in extra- cellular and intracellular compartments is LEAST accurate?
a. Extracellular sodium ion concentration is approximately 140 mM (140 mEq/l)
b. Intracellular potassium ion concentration is approximately 160 mmol/l (160 mEq/L)
c. Extracellular chloride ion concentration is
approximately 110 mM (110 mEq/l)
d. Intracellular calcium ion concentration is
approximately 2 mM (4 mEq/l)
e. Extracellular bicarbonate ion concentra-
tion is approximately 22-26 mmol/l

Answer 5

d. Intracellular calcium ion concentration is
approximately 2 mM (4 mEq/l)

Question 6

Which one of the following statements concerning the resting membrane potential is most accurate?
a. Maintenance of the resting membrane potential is an energy dependent process requiring Na/K-ATPase
b. A membrane is depolarized when there is an increase in separation of the charge across it from baseline
c. Neurons become depolarized when the charge inside the cell becomes more negative compared to its resting state
d. Hyperpolarization of a cell membrane occurs when the outside of the cell becomes more negatively charged com- pared to its resting state
e. Resting potential difference across a membrane is not dependent on the sepa- ration of charged ions across it

Answer 6

a. Maintenance of the resting membrane potential is an energy dependent process requiring Na/K-ATPase

The voltage, or potential difference, across the cell membrane (resting membrane potential) is a result of the separation of positively and nega- tively charged ions across it, the balance of which is actively maintained by ATP-dependent mem- brane pumps. At rest, the inside of a cell holds more negative charge than the extracellular fluid outside it. Membrane depolarization is said to occur when the separation of charge across the membrane is reduced from the resting/baseline value (i.e., the inside of cell becomes more posi- tively charged), whereas hyperpolarization is said to occur if the separation of charge is increased (i.e., the inside of the cell becomes more nega- tively charged than at rest). There is a tendency for ions to passively leak in or out of the cell against their respective electrochemical gradi- ents, hence the requirement for continuously active ATP-dependent membrane pumps to pre- vent an overall change in the resting membrane potential. The propensity for ion flux across the membrane passively down artificially membrane pump produced and maintained electrochemical gradients is exploited and forms the basis for action potentials during which ion channels open up to allow passive ion flux on a magnitude and time scale at which ATP-dependent membrane pumps cannot prevent, allowing depolarization/ hyperpolarization to act as a high fidelity way of information transfer.

Question 7

Which one of the following statements
regarding ion channels is LEAST accurate?
a. Nicotinic AChR is a ligand-gated ion
channel
b. NMDA receptor is a ligand-gated cation
channel
c. Voltage-gated sodium channels open in
response to hyperpolarization of the cell
membrane
d. Cyclic AMP is generated by activation of
beta-adrenoceptors
e. GABA-B receptor is a ligand-gated ion channel

Answer 7

e. GABA-B receptor is a ligand-gated ion channel

Ion channels are transmembrane proteins that permit the selective passage of ions with specific characteristics (size and charge) down their elec- trochemical gradient by passive diffusion when open. Ion channels are controlled by gates, and, depending on the position of the gates, the chan- nels may be open or closed. The higher the prob- ability that the channel is open, the higher is its conductance or permeability. The gates on ion channels are controlled by three types of sensors:
* Voltage-gated channels have gates that are controlled by changes in membrane potential.
* Second messenger-gated channels have gates that are controlled by changes in levels of intracellular signaling molecules such as cyclic AMP (e.g., beta-adrenoceptors, alpha2-adrenoceptors, M2 muscarinic AChR) or inositol 1,4,5-triphosphate (IP3; e.g., alpha1-adrenoceptors, M1/M3 musca- rinic AChR). In general, Gs/Gi G-protein coupled receptor activation causes adenylyl cyclase to convert ATP to cAMP, which then activates protein kinase A to phosphorylate downstream proteins. In contrast, Gq G- protein coupled receptors cause activation of phospholipase C which hydrolyzes mem- brane phospholipid (phosphatidylinositol 4,5-bisphosphate; PIP2) to diacyl glycerol (DAG) and inositol 1,4,5-trisphosphate (IP3).
* Ligand-gated channels have gates that are controlled by hormones and neurotrans- mitters. The sensors for these gates are located on the extra-cellular side of the ion channel (e.g., nicotinic AChR allows Na+ and K+ passage on binding acetylcholine).

Question 8

Which one of the following statements
regarding the membrane potentials is most
accurate?
a. The Nernst equation can be used to calculate the resting membrane potential of
a cell
b. The Goldman equation can be used to
calculate the intracellular concentration
of sodium
c. The equilibrium potential for potassium
is approximately +70 mV
d. Equilibrium potential of an ion maintains
a unique ion gradient for it exists across a
cell membrane
e. At electrochemical equilibrium, the chemical and electrical driving forces acting on an ion are equal and opposite, and no further net diffusion occurs

Answer 8

e. At electrochemical equilibrium, the chemical and electrical driving forces acting on an ion are equal and opposite, and no further net diffusion occurs

The concept of equilibrium potential is simply an extension of the concept of diffusion potential. If there is a concentration difference for an ion across a membrane and the membrane is permeable to that ion, a potential difference (the diffusion potential) is created. Eventually, net diffusion of the ion slows and then stops because of that potential difference. In other words, if a cation diffuses down its concen- tration gradient, it carries a positive charge across the membrane, which will retard and eventually
stop further diffusion of the cation. Equally, if an anion diffuses down its concentration gradient, it carries a negative charge, which will retard and then stop further diffusion of the anion. The equilibrium potential is the diffusion potential that exactly bal- ances or opposes the tendency for diffusion down the concentration difference. At electrochemical equilibrium, the chemical and electrical driving forces acting on an ion are equal and opposite, and no further net diffusion occurs. The Nernst equation is used to calculate the equilibrium poten- tial for an ion at a given concentration difference across a membrane, assuming that the membrane is permeable to that ion. By definition, the equilib- rium potential is calculated for one ion at a time. For a given ion X with charge z at 37 °C, the equilibrium potential (Ex) 1⁄4 (60/z) log10([intracellular con- centration of X in mmol/l]/[extracellular concen- tration of X in mmol/l]). For example, E(Na)1⁄4 (60/+1) log10(10/140) 1⁄4 + 68.8 mV. Whereas for E(k) 1⁄4 (60/+1) log10 (140/10) 1⁄4 87 mV. The Goldmann equation can be used to calculate the exact resting membrane potential based on all the permeable ions across it, but in practice since in neurons 80% of conductance is due to K+ (resid- ual is 15% due to Na+ and 5% due to Cl), the rest- ing membrane voltage (Vm) of approximately 70 mV is much closer to that of the equilibrium potential for K+.

Question 9

Which one of the following best describes ions
responsible for membrane hyperpolarization?
a. Chloride and sodium
b. Chloride and potassium
c. Potassium and sodium
d. Sodium and calcium
e. Sodium only

Answer 9

b. Chloride and potassium

Assuming normal intracellular and extracellular concentrations of ions, both potassium and chlo- ride ions have a negative equilibrium potential hence will result in hyperpolarization of the cell if allowed to flow down their electrochemical gradients. Chloride influx into the cell down its electrochemical gradient results in a gain of negative charge, whereas efflux of potassium reflects a loss of positive charge in the intracellu- lar compartment to achieve this. Physiological electrochemical gradients for both sodium and calcium favor influx into the cell, and would cause depolarization due to net gain of positive charge.

Question 10

Which one of the following statements
regarding the passive membrane properties
of neurons is LEAST accurate?
a. The length constant is the distance where
the initial voltage response to current flow
decays to 1/e (or 37%) of its value
b. Smaller length constant means passive
flow of an action potential will stop at a
shorter distance along an axon
c. Length constant is greater in unmyelinated and large diameter axons
d. The time constant is a function of the
membrane’s resistance and capacitance
e. The time constant characterizes how rap-
idly current flow changes the membrane
potential

Answer 10

c. Length constant is greater in unmyelinated and large diameter axons

The passive flow of electrical current plays a cen- tral role in action potential propagation, synaptic transmission, and all other forms of electrical sig- naling in nerve cells. For the case of a cylindrical axon, subthreshold current injected into one part of the axon spreads passively along the axon until
the current is dissipated (decays) by leakage out
across the axon membrane. The decrement in
the current flow with distance is described by a
simple exponential function: Vx1⁄4V0ex/λ where
Vx is the voltage response at any distance x along
the axon, V0 is the voltage change at the point
where current is injected into the axon, e is the base
of natural logarithms (%2.7), and λ is the length
constant of the axon. As evident in this relation-
ship, the length constant is the distance where
the initial voltage response (V0) decays to 1/e (or
37%) of its value. The length constant is thus a
way to characterize how far passive current flow
spreads before it leaks out of the axon, with leakier
axons having shorter length constants. The length
constant depends upon the physical properties of
the axon, in particular the relative resistances of
the plasma membrane (Rm), the intracellular axo-
plasm (Ri), and the extracellular medium (R0).
The relationship between these parameters is:
λ 1⁄4 √(Rm/[R0+Ri]). Hence, to improve the passive
flow of current along an axon (i.e., slow the rate of
decay), the resistance of the plasma membrane
should be as high as possible (e.g., myelination)
and the resistances of the axoplasm and extracellu-
lar medium should be low. Another important
consequence of the passive properties of neurons
is that currents flowing across a membrane do
not immediately change the membrane potential.
These delays in changing the membrane potential
are due to the fact that the plasma membrane
behaves as a capacitor, storing the initial charge
that flows at the beginning and end of the current
pulse. For the case of a cell whose membrane
potential is spatially uniform, the change in the
membrane potential at any time, Vt, after begin-
ning the current pulse can also be described by
an exponential relationship: V 1⁄4V (1et/τ) t1
where V1 is the steady-state value of the mem- brane potential change, t is the time after the cur- rent pulse begins, and τ is the membrane time constant. The time constant is thus defined as the time when the voltage response (Vt) rises to 1(1/e) (or 63%) of V1. After the current pulse ends, the membrane potential change also declines exponentially according to the relationship Vt1⁄4V1et/τ During this decay, the membrane potential returns to 1/e of V1 at a time equal to t. The time constant characterizes how rapidly current flow changes the membrane potential. The membrane time constant also depends on the physical properties of the nerve cell, specifically on the resistance (Rm) and capacitance (Cm) of the
plasma membrane such that: τ 1⁄4 RmCm. The values of Rm and Cm depend, in part, on the size of the neu- ron, with larger cells having lower resistances and larger capacitances. In general, small nerve cells tend to have long time constants and large cells brief time constants. Regarding achieving threshold for action potential generation, long time constants favor temporal summation of EPSPs, whereas short time constant allows coincidence detection through spatial summation of EPSPs/IPSPs.

Question 11

Which one of the following statements
regarding the generation of the action potential is LEAST accurate?
a. It is an all-or-nothing, regenerative wave
of depolarization
b. It can propagate bidirectionally
c. Repolarization is due to inactivation of
sodium channels combined with increased
conductance in potassium channels
d. Hyperpolarization occurs due to increases
in potassium conductance lasting beyond
the point of return to resting membrane
potential
e. Repolarization is required for inactivated
sodium channels to return to the closed state

Answer 11

b. It can propagate bidirectionally

The action potential, as classically defined, is an all-or-nothing, regenerative, directionally propa- gated, depolarizing nerve impulse. At rest, the membrane has high K+ conductance and Vm is near the Nernst equilibrium potential for K+ (EK). Spread of an action potential from an adja- cent area of the membrane brings the membrane potential Em, to a threshold potential (approxi- mately 40 to 55 mV) causing a large increase in Na+ conductance of the membrane and Na+ influx such that Vm approaches the Nernst poten- tial for Na+ (ENa) and the membrane depolarizes. Depolarization causes voltage-gated sodium channels to change from an open to an inactivated state, preventing further rises in membrane potential, and at the same time there is an increase in conductance of delayed-rectifier K channels causing K efflux and movement of Vm towards the equilibrium potential for potassium (repolar- ization). This increased K+ conductance usually lasts slightly longer than the time required to bring the membrane potential back to its normal resting level, hence there is an overshoot (hyper- polarization) which subsequently decays. An absolute refractory period for action potential fir- ing is seen when sodium channels are in their inactivated state, but as repolarization progresses more Na channels move from an inactivated to a close state, and thus could be reopened in the presence of a supratheshold stimulus (relative refractory period). The figure below shows the action potential (yellow), and underlying changes in membrane conductance to sodium (purple) and potassium (red) due to opening/inactivation of channels.

Question 12

Which one of the following sites acts as the
trigger zone that integrates incoming signals
from other cells and initiates the action
potential?
a. Soma
b. Dendritic shaft
c. Dendritic spines
d. Axon hillock and initial segment
e. Axon trunk

Answer 12

d. Axon hillock and initial segment

Question 13

Which one of the following statements
regarding phenomena relevant to action
potential conduction is LEAST accurate?
a. Accommodation is dependent on postsynaptic receptor phagocytosis
b. Saltatory conduction occurs to high resistance to transmembrane current leak in myelinated segments of nerve
c. Absolute refractory period is due to inactivation of voltage-gated sodium channels
d. Relative refractory period occurs when
populations of inactivated voltage-gated
sodium channels return to the closed state
e. Unidirectional propagation is function of the refractory periods associated with
action potentials

Answer 13

a. Accommodation is dependent on postsynaptic receptor phagocytosis

Unidirectional propagation is due to the inactive state of the sodium channel, and this wave of inactivation immediately following the action potential prevents it from reversing direction. Accommodation occurs when subthreshold stim- ulus will stimulate channels to open, but at a rate that is too slow for there to be a sufficient number of open channels at any one time to fire an AP but sufficient for channel inactivation. Absolute refractory period is the time period immediately after/during the action potential upstroke when most of the neuron’s sodium channels are inacti- vated and cannot be opened to elicit a second action potential. The relative refractory period refers to the period during repolarization when inactivated Na channels return to a closed state and a second action potential can be generated but is more difficult than normal (becomes pro- gressively less difficult to elicit an action potential during the relative refractory period until it returns to normal). Myelination of axons involves wrapping the axon in myelin, which consists of multiple layers of closely opposed glial cell mem- branes (i.e., oligodendrocytes in CNS, Schwann cells in PNS). Myelination electrically insulates the axonal membrane, reducing the ability of cur- rent to leak out of the axon and thus increasing the distance along the axon that a given local current can flow passively such that the time- consuming process of action potential generation occurs only at specific points along the axon, called nodes of Ranvier, where there is a gap in the myelin wrapping (rather than adjacent mem- brane in a depolarization wave). As it happens, an action potential generated at one node of Ranvier elicits current that flows passively within the axo- plasm of the myelinated segment until the next node is reached and another action potential is generated, and the cycle is repeated along the length of the axon. Because current flows across the neuronal membrane only at the nodes, action potentials “leap” from node to node and this is termed salutatory conduction. Myelination greatly speeds up action potential conduction (velocities up to 150 m/s) compared to unmyelin- ated axons (0.5-10 m/s). (In: Purves D, et al. (Eds.), Neuroscience, 3rd ed. MA: Sinauer.)

Question 14

Which one of the following synapse types is
characterized by gap junctions?
a. Axodendritic synapses
b. Axoaxonic synapses
c. Axosomatic synapses
d. Dendrodendritic synapses
e. Electrical synapses

Answer 14

e. Electrical synapses

ity of synapses (e.g., some neuroendocrine cells in hypothalamus) and are characterized by very closely apposed pre and post-synaptic membranes connected by a gap junction. These junctions contain aligned paired channels so that each paired channel forms a pore (larger than those observed in ligand-gated channels) and allows for the bidirectional transmission. Chemical syn- apse types include:
Axosecretory—axon terminal secretes directly into bloodstream (e.g., hypothalamus)
Axodendritic—axon terminal ends on den- dritic spines or shaft (type I excitatory synapse)
Axoaxonic—axon terminal secretes onto another axon
Axoextracellular—axon with no connection secretes into extracellular fluid
Axosomatic—axon terminal ends on cell soma (type II inhibitory synapse, e.g., basket cell onto Purkinje cell)
Axosynaptic—axon terminal ends on presyn- aptic terminal of another axon

Question 15

Which one of the following statements
regarding neurotransmission at chemical
synapses is LEAST accurate?
a. The action potential stimulates the postsynaptic terminal to release neurotransmitter
b. Release of the transmitter into the synaptic
cleft by exocytosis is triggered by an influx
of Ca2+ through voltage-gated channels
c. Postsynaptic current produces an excit-
atory or inhibitory postsynaptic potential
d. Neurotransmitters may undergo degrada-
tion in the synaptic cleft or be transported
back into the presynaptic terminal
e. Vesicular membrane is retrieved from the
plasma membrane after exocytosis

Answer 15

a. The action potential stimulates the
postsynaptic terminal to release
neurotransmitter

Neurotransmission at a chemical synapse requires a neurotransmitter to be synthesized and stored in the presynaptic vesicles. The arrival of an action potential at the presynaptic terminal results in depolarization dependent opening of voltage-gated Ca2+ channels and calcium influx. Then, there is Ca2+ through these channels, causing the vesicles to fuse with the presynaptic membrane in a mechanism mediated by synapto- tagmin 1 and SNAP-25 (SNARE) calcium sensi- tive proteins. The transmitter is then released into the presynaptic cleft (by exocytosis) and binds to receptor molecules in the postsynaptic membrane. This leads to the opening or closing of postsynaptic channels. The resultant current results in an EPSP or IPSP, which causes a change in excitability of the postsynaptic cell. The vesicular membrane is then retrieved from the plasma membrane by endocytosis. If summa- tion of EPSPs or IPSPs exceeds threshold poten- tial at the axon hillock, an axon potential is generated. To prevent repetitive stimulation, neurotransmitters are either degraded in the pre- synaptic cleft or taken up by endocytosis in presynaptic cell.

Question 16

Which one of the following statements
regarding cholinergic neurotransmission is
LEAST likely?
a. synthesized in nerve terminals from the
precursors acetyl coenzyme A
b. acetylcholinesterase (AChE) hydrolysis
Ach into acetate and choline
c. Nicotinic AChR are a nonselective cation
channel complex consisting of five subunits
arranged around a central membrane-
spanning pore
d. α-bungarotoxin binds to muscarinic AChRs
e. mAChRs are metabotropic G-protein
coupled receptors

Answer 16

d. α-bungarotoxin binds to muscarinic AChRs

In addition to the action of ACh as the neuro- transmitter at skeletal neuromuscular junctions as well as the neuromuscular synapse between the vagus nerve and cardiac muscle fibers, ACh serves as a transmitter at synapses in the ganglia of the visceral motor system, and at a variety of sites within the central nervous system. Acetyl- choline is synthesized in nerve terminals from the precursors acetyl coenzyme A (acetyl CoA, which is synthesized from glucose) and choline, in a reaction catalyzed by choline acetyltransfer- ase (CAT). Choline is present in plasma at a high concentration (about 10 mM) and is taken up into cholinergic neurons by a high-affinity Na+/cho- line transporter. After synthesis in the cytoplasm of the neuron, a vesicular ACh transporter loads approximately 10,000 molecules of ACh into each cholinergic vesicle. The postsynaptic actions of ACh at many cholinergic synapses terminated by acetylcholinesterase (AChE) hydrolysis Ach into acetate and choline. The choline produced by ACh hydrolysis is transported back into nerve terminals and used to resynthesize ACh. Many of the postsynaptic actions of ACh are mediated by the nicotinic ACh receptor nAChR which is a nonselective cation channels that generate excit- atory postsynaptic responses a large protein com- plex consisting of five subunits arranged around a central membrane-spanning pore. In the case of skeletal muscle AChRs, the receptor pentamer contains two α subunits, each of which binds one molecule of ACh. Because both ACh-binding sites must be occupied for the channel to open, only relatively high concentrations of this neuro- transmitter lead to channel activation. These
subunits also bind other ligands, such as nicotine and α-bungarotoxin. At the neuromuscular junc- tion, the two α subunits are combined with up to four other types of subunit—β, γ, δ, ε—in the ratio 2α:β:ε:δ. Neuronal nAChRs typically differ from those of muscle in that they lack sensitivity to α-bungarotoxin, and comprise only two recep- tor subunit types (α and β), which are present in a ratio of 3α:2β. In all cases, however, five individ- ual subunits assemble to form a functional, cation-selective nACh receptor. Each subunit of the nAChR molecule contains four transmem- brane domains that make up the ion channel por- tion of the receptor, and a long extracellular region that makes up the ACh-binding domain. A second type of ACh receptors is activated by muscarine and thus they are referred to as mus- carinic ACh receptors (mAChRs). mAChRs are metabotropic and mediate most of the effects of ACh in brain via G-protein signaling. Several subtypes of mAChR are known. Muscarinic ACh receptors are highly expressed in the stria- tum and various other forebrain regions, where they exert an inhibitory influence on dopamine- mediated motor effects. These receptors are also found in the ganglia of the peripheral nervous system and autonomic effector organs—such as heart, smooth muscle, and exocrine glands— and are responsible for the inhibition of heart rate by the vagus nerve. Nevertheless, mACh blockers that are therapeutically useful include atropine (used to dilate the pupil), scopolamine (effective in preventing motion sickness), and ipratropium (useful in the treatment of asthma). (In: Purves D, et al. (Eds.) Neuroscience 3rd ed. MA: Sinauer.)

Question 17

Which one of the following statements
regarding glutamatergic neurotransmission
is LEAST accurate?
a. At depolarized membrane potentials, an
Mg2+ blocks the pore of the NMDA
receptor
b. most prevalent precursor for glutamate
synthesis is glutamine
c. glutamine is taken up into presynaptic ter-
minals and metabolized to glutamate by
the mitochondrial enzyme glutaminase
d. Activation of metabotropic GluRs leads to
inhibition of postsynaptic Ca2+ and Na+
channels
e. AMPA receptors are a type of metabotropic GluR

Answer 17

e. AMPA receptors are a type of metabotropic GluR

Nearly all excitatory neurons in the central ner- vous system are glutamatergic, and it is estimated that over half of all brain synapses release this agent and cause excitotocity in ischemic brain. Glutamate is a nonessential amino acid that does not cross the blood-brain barrier and therefore must be synthesized in neurons from local pre- cursors. The most prevalent precursor for gluta- mate synthesis is glutamine, which is released by glial cells. Once released, glutamine is taken up into presynaptic terminals and metabolized to glutamate by the mitochondrial enzyme gluta- minase. Glutamate can also be synthesized by transamination of 2-oxoglutarate, an intermedi- ate of the tricarboxylic acid cycle. Hence, some of the glucose metabolized by neurons can also be used for glutamate synthesis. The glutamate synthesized in the presynaptic cytoplasm is pack- aged into synaptic vesicles by transporters, termed VGLUT. Once released, glutamate is removed from the synaptic cleft by the excitatory amino acid transporters (EAATs). Glutamate taken up by glial cells is converted into glutamine by the enzyme glutamine synthetase; glutamine is then transported out of the glial cells and into nerve terminals. In this way, synaptic terminals cooperate with glial cells to maintain an adequate supply of the neurotransmitter. This overall sequence of events is referred to as the glutamate-glutamine cycle. Receptors of these are ionotropic receptors called, respectively, NMDA receptors, AMPA receptors, and kainate receptors. These glutamate receptors are named after the agonists that activate them: NMDA (N-methyl-D-aspartate), AMPA (α-amino-3- hydroxyl-5-methyl-4-isoxazole-propionate), and kainic acid. All of the ionotropic glutamate recep- tors are nonselective cation channels similar to the nAChR, allowing the passage of Na+ and K+, and in some cases small amounts of Ca2+. NMDA receptor ion channels allow the entry of Ca2+ in addition to monovalent cations such as Na+ and K+. As a result, EPSPs produced by NMDA receptors can increase the concentration of Ca2+ within the postsynaptic neuron; the Ca2+ concentration change can then act as a second messenger to activate intracellular signaling cas- cades. Another key property is that they bind extracellular Mg2+. At hyperpolarized membrane potentials, this ion blocks the pore of the NMDA receptor channel. Depolarization, however, pushes Mg2+ out of the pore, allowing other cat- ions to flow. This property provides the basis for a voltage-dependence to current flow through the receptor and means that NMDA receptors pass cations (most notably Ca2+) only during depolar- ization of the postsynaptic cell, due to either acti- vation of a large number of excitatory inputs and/ or by repetitive firing of action potentials in the presynaptic cell. These properties are widely thought to be the basis for some forms of infor- mation storage at synapses, such as memory. Another unusual property of NMRA receptors is that opening the channel of this receptor requires the presence of a coagonist, the amino acid glycine. In addition to these ionotropic glu- tamate receptors, there are three types of metabo- tropic glutamate receptor (mGluRs). These receptors, which modulate postsynaptic ion chan- nels indirectly, differ in their coupling to intracel- lular signal transduction pathways and in their sensitivity to pharmacological agents. Activation of many of these receptors leads to inhibition of postsynaptic Ca2+ and Na+ channels. Unlike the
excitatory ionotropic glutamate receptors, mGluRs cause slower postsynaptic responses that can either increase or decrease the excitability of postsynaptic cells. (In: Purves D, et al. (Eds.) Neuroscience 3rd ed. MA: Sinauer.)

Question 18

Which one of the following enzymatic con-
version pathways is LEAST accurate?
a. Tyrosine-tyrosine hydroxylase-DOPA
(dihydroxyphenylalanine)
b. DOPA-catechol O-methyltransferase-
dopamine
c. Histidine-histidine decarboxylase-
Histamine
d. Dopamine-Dopamine beta-hydroxylase-
Norepinephrine
e. Tryptophan is converted to serotonin
by tryptophan 5-hydroxylase and a
decarboxylase

Answer 18

b. DOPA-catechol O-methyltransferase-
dopamine

There are five well-established biogenic amine neurotransmitters: the three catecholamines— dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline)—and histamine and serotonin. Their synthesis is as follows:
* Tyrosine-tyrosine hydroxylase-DOPA (dihydroxyphenylalanine)
* DOPA-DOPA decarboxylase-dopamine
* Dopamine-Dopamine beta-hydroxylase-
Norepinephrine
* Norepinephrine-Phenylethanolamine N-
methyltransferase-Epinephrine
* Histidine-histidine decarboxylase-Histamine * Tryptophan-tryptophan 5-hydroxylase-
5-hydroxytryptophan-Aromatic L-amino acid decarboxylase-Serotonin (5-Hydroxy tryptamine)

Question 19

Which one of the following statements
regarding dopaminergic neurotransmission
is LEAST accurate?
a. Dopamine is loaded into synaptic vesicles
via a vesicular monoamine transporter
(VMAT)
b. The neostriatum is the major site of dopa-minergic transmission in the brain
c. Dopamine is derived from norepinephrine
d. Cocaine inhibits the Na-dependent dopamine transporter
e. monoamine oxidase (MAO) and catechol
O-methyltransferase (COMT)

Answer 19

c. Dopamine is derived from norepinephrine

Dopamine is present in several brain regions, although the major dopamine-containing area of the brain is the corpus striatum, which receives major input from the substantia nigra and plays an essential role in the coordination of body move- ments. Dopamine is also believed to be involved in motivation, reward, and reinforcement, and many drugs of abuse work by affecting dopami- nergic synapses in the CNS. In addition to these roles in the CNS, dopamine also plays a poorly understood role in some sympathetic ganglia. Dopamine is produced by the action of DOPA decarboxylase on DOPA. Following its synthesis in the cytoplasm of presynaptic terminals, dopa- mine is loaded into synaptic vesicles via a vesicular monoamine transporter (VMAT). Dopamine action in the synaptic cleft is terminated by reup- take of dopamine into nerve terminals or surrounding glial cells by a Na+-dependent dopa- mine transporter, termed DAT. Cocaine appar- ently produces its psychotropic effects by binding to and inhibiting DAT, yielding a net increase in dopamine release from specific brain areas. Amphetamine, another addictive drug, also inhibits DAT as well as the transporter for norepinephrine (see below). The two major enzymes involved in the catabolism of dopamine
are monoamine oxidase (MAO) and catechol O-methyltransferase (COMT). Both neurons and glia contain mitochondrial MAO and cyto- plasmic COMT. Inhibitors of these enzymes, such as phenelzine and tranylcypromine, are used clinically as antidepressants. Once released, dopamine acts exclusively by activating G-pro- tein-coupled receptors. Most dopamine receptor subtypes act by either activating or inhibiting adenylyl cyclase. Activation of these receptors generally contribute to complex behaviors; for example, administration of dopamine receptor agonists elicits hyperactivity and repetitive, ste- reotyped behavior in laboratory animals. Activa- tion of another type of dopamine receptor in the medulla inhibits vomiting. Thus, antagonists of these receptors are used as emetics to induce vomiting after poisoning or a drug overdose. Dopamine receptor antagonists can also elicit catalepsy, a state in which it is difficult to ini- tiate voluntary motor movement, suggesting a basis for this aspect of some psychoses. (In: Purves D, et al. (Eds.) Neuroscience 3rd ed. MA: Sinauer.)

Question 20

Which one of the following statements
regarding GABAergic neurotransmission is
LEAST accurate?
a. Glutamic acid decarboxylase (GAD) conversion of glutamate to GABA
b. Vitamin B6 is important in the function of glutamic acid decarboxylase
c. The mechanism of GABA removal from the synaptic cleft is similar to that for glutamate
d. GABAA and GABAC receptors are iono tropic receptors and are Ca2+ conductors
e. GABAB receptors are metabotropic and
increase K conductance

Answer 20

d. GABAA and GABAC receptors are iono tropic receptors and are Ca2+ conductors

cord use either γ-aminobutyric acid (GABA) or glycine as neurotransmitters. It is now known that as many as a third of the synapses in the brain use GABA as their inhibitory neurotrans- mitter. GABA is most commonly found in local circuit interneurons, although cerebellar Pur- kinje cells provide an example of a GABAergic projection neuron. The predominant precursor for GABA synthesis is glucose, which is metabo- lized to glutamate by the tricarboxylic acid cycle enzymes (pyruvate and glutamine can also act as precursors). The enzyme glutamic acid decar- boxylase (GAD), which is found almost exclu- sively in GABAergic neurons, catalyzes the conversion of glutamate to GABA. GAD requires a cofactor, pyridoxal phosphate, for activity. Because pyridoxal phosphate is derived from vitamin B6, a B6 deficiency can lead to diminished GABA synthesis. Once GABA is syn- thesized, it is transported into synaptic vesicles via a vesicular inhibitory amino acid transporter (VIATT). The mechanism of GABA removal is similar to that for glutamate: Both neurons and glia contain high-affinity transporters for GABA, termed GATs. Most GABA is eventually con- verted to succinate, which is metabolized further in the tricarboxylic acid cycle that mediates cel- lular ATP synthesis. The enzymes required for
this degradation, GABA transaminase and succi- nic semialdehyde dehydrogenase, are mitochon- drial enzymes. Inhibitory synapses employing GABA as their transmitter can exhibit three types of postsynaptic receptors, called GABAA, GABAB, and GABAC. GABAA and GABAC receptors are ionotropic receptors, while GABAB receptors are metabotropic. The iono- tropic GABA receptors are usually inhibitory because their associated channels are permeable to Cl; the flow of the negatively charged chlo- ride ions inhibits postsynaptic cells since the reversal potential for Cl is more negative than the threshold for neuronal firing. Like other ionotropic receptors, GABA receptors are penta- mers assembled from a combination of five types of subunits (αβγδρ). Benzodiazepines, such as diazepam and chlordiazepoxide, are tranquilizing (anxiety reducing) drugs that enhance GABAer- gic transmission by binding to the α and δ sub- units of GABAA receptors. Metabotropic GABA receptors (GABAB) are also widely distributed in brain. Like the ionotropic GABAA receptors, GABAB receptors are inhibitory. Rather than activating Cl selective channels, however, GABAB-mediated inhibition is due to the activa- tion of K+ channels. A second mechanism for GABAB-mediated inhibition is by blocking Ca2+ channels, which tends to hyperpolarize pos- tsynaptic cells. Unlike most metabotropic recep- tors, GABAB receptors appear to assemble as heterodimers of GABAB R1 and R2 subunits. (In: Purves D, et al. (Eds.) Neuroscience 3rd ed. MA: Sinauer.)

Question 21

Which one of the following areas does the superior temporal gyrus (Heschl’s gyrus) primarily receive inputs from?
a. Centromedian thalamic nucleus
b. Medial geniculate thalamic nucleus
c. Dorsomedial thalamic nucleus
d. Anterior thalamic nucleus
e. Centromedian-parafascicular nucleus

Answer 21

b. Medial geniculate thalamic nucleus

Question 22

Which one of the following cell types
involved in vision is able to generate an action
potential?
a. Ganglion cells
b. Bipolar cells
c. Horizontal cells
d. Rods and cones
e. Amacrine cells

Answer 22

a. Ganglion cells

The output of the retina is determined by gan- glion cells which can generate action potentials and give rise to optic nerve. The other cell types display graded depolarizing/hyperpolarizing responses and amacrine cells show calcium spikes. In general, 99% of all ganglion cells are con- cerned with details of image formation and receive input from rods and cones via synaptic relays through the layers of the retina, are involved in circadian rhythms and the pupillary light reflex. The second type, melanopsin- containing ganglion cells, comprise less than 1% of all ganglion cells, are intrinsically sensitive to light and will generate action potentials (even without rods/cones, particularly blue light); are not concerned with image formation, and have connections to the suprachiasmatic and pretectal nuclei maintaining circadian rhythm. This type of ganglion cell explains why those blind due to rod/ cone disease (e.g., retinitis pigmentosa) may still have an intact pupillary reflex and maintain circa- dian rhythm.

Question 23

Which one of the following statements
regarding cones and rods is LEAST accurate?
a. In the dark, rods have a high resting membrane potential of about -70 mV
b. In the dark, both rods and cones tonically release glutamate onto synapsing
bipolar cells
c. Photon absorption by rhodopsin results in
reduced cyclic GMP and hyperpolarization of the rod cell
d. Photon absorption by cone opsin results
in reduced cyclic GMP and hyperpolarization of the rod cell
e. Reduced glutamate secretion can cause
both hyperpolarization or depolarization
in bipolar cells

Answer 23

a. In the dark, rods have a high resting membrane potential of about -70 mV

Rod cells are named for the shape of their outer segment, which is a membrane-bound cylinder containing hundreds of tightly stacked membra- nous discs. In the dark, cGMP levels in the rod outer segment are high facilitating a inward Na and Ca current results in a relatively high resting membrane potential for rod cells, about 40 mV, and at the rod spherule there is tonic release of glutamate. With light, rhodopsin absorbs photons and undergoes a conformational change causing reduced levels of cGMP, causing closure of sodium channels, a wave of hyperpo- larization and a transient reduction in this tonic release of glutamate. Cone outer segments also consist of a membranous stack of constantly decreasing diameter (from cilium to tip), giving the cell its characteristic shape. Cone opsin absorbs photons and undergoes a conformational change, resulting in a hyperpolarization of the cell membrane. This hyperpolarization propa- gates passively to the cone’s synaptic ending, the cone pedicle, in the outer plexiform layer. Like rods, cones release the neurotransmitter glutamate tonically in the dark and respond to light with a decrease in glutamate release. There are three types of cones, each tuned to a different light wavelength. L-cones (red cones) are sensi- tive to long wavelengths, M-cones (green cones) to medium wavelengths, and S-cones (blue cones) to short wavelengths. Because any pure color represents a particular wavelength of light, each color will be represented by a unique com- bination of responses in the L-, M-, and S-cones. At the posterior pole of the eye is a yellowish spot, the macula lutea, the center of which is a depression called the fovea centralis Cones, which are responsible for color vision, are the only type of photoreceptor present in the fovea. In contrast, rods, which are most sensitive at low levels of illumination, are the predominant pho- toreceptors in the periphery of the retina. The visual world is a composite formed from a suc- cession of foveal images carrying form and color information supplemented with input from the peripheral retina carrying motion information. Several adaptations of the fovea allow it to medi- ate the highest visual acuity in the retina. Neu- rons of the inner layer of retina are actually displaced laterally to the side of the fovea to
minimize light scattering on the way to the receptors. In addition, within the fovea, the ratio of photoreceptors to ganglion cells falls dramat- ically. Most foveal receptors synapse on only one bipolar cell, which synapses on only one gan- glion cell. Because each ganglion cell is devoted to a very small portion of the visual field, central vision has high resolution. In other words, the receptive field of a foveal ganglion cell (i.e., the region of stimulus space that can activate it) is small. At the periphery, the ratio of recep- tors to ganglion cells is high; thus, each ganglion cell has a large receptive field. The large recep- tive field reduces the spatial resolution of the peripheral portion of the retina but increases its sensitivity because more photoreceptors col- lect light for a ganglion cell. Lastly, the magni- tude of phototransduction amplification varies with the prevailing levels of illumination (light adaptation). At low levels of illumination, photo- receptors are the most sensitive to light. As levels of illumination increase, sensitivity decreases (due to reduction in calcium currents in the rod outer segment), preventing the receptors from saturating and thereby greatly extending the range of light intensities over which they operate.

Question 24

Which one of the following events during visual processing is LEAST accurate?
a. The on-center bipolar depolarizes in response to reduced tonic glutamate release
b. The on-center ganglion cell will produce a burst of action potentials if a spot of light is shone on the receptive field center
c. The ganglion cell that receives its input from an off-center bipolar cell will reduce its firing rate in response a spot of light is shone on the receptive field center
d. The receptive fields of on-center and off-center ganglion cells do not overlap
e. Glutamate released from a cone cell has differential effect in different cells with which it synapses

Answer 24

d. The receptive fields of on-center and off-center ganglion cells do not overlap

Most of the information in visual scenes consists of spatial variations in light intensity. Each gan- glion cell responds to stimulation of a small cir- cular patch of the retina, which defines the cell’s receptive field. Turning on a spot of light in the receptive field center of an on-center ganglion cell produces a burst of action potentials. The same stimulus applied to the receptive field cen- ter of an off-center ganglion cell reduces the rate of discharge, and when the spot of light is turned off, the cell responds with a burst of action potentials. Complementary patterns of activity are also found for on-center versus off-center cell type when a dark spot is placed in the recep- tive field center. Thus, on-center cells increase their discharge rate to luminance increments in the receptive field center, whereas off-center cells increase their discharge rate to luminance decrements in the receptive field center. On- and off-center ganglion cells are present in roughly equal numbers. Their receptive fields have overlapping distributions, so that every point on the retinal surface (i.e., every part of visual space) is analyzed by several on-center and several off-center ganglion cells. In practice, silencing on-center ganglion cells in primates
caused a deficit in their ability to detect stimuli that were brighter than the background; how- ever, they could still see objects that were darker than the background. These observations imply that information about increases or decreases in luminance is carried separately to the brain by the axons of these two different types of ret- inal ganglion cells. Having separate luminance “channels” means that changes in light intensity, whether increases or decreases, are always con- veyed to the brain by an increased number of action potentials. Because ganglion cells rapidly adapt to changes in luminance, their “resting” discharge rate in constant illumination is rela- tively low. Although an increase in discharge rate above resting level serves as a reliable signal, a decrease in firing rate from an initially low rate of discharge might not. Thus, having luminance changes signaled by two classes of adaptable cells provides unambiguous information about both luminance increments and decrements. On- and off-center ganglion cells have dendrites that arborize in separate strata of the inner plexiform layer, forming synapses selectively with the ter- minals of on- and off-center bipolar cells that respond to luminance increases and decreases, respectively. As mentioned previously, the prin- cipal difference between ganglion cells and bipo- lar cells lies in the nature of their electrical response. Like most other cells in the retina, bipolar cells have graded potentials rather than action potentials. Graded depolarization of bipo- lar cells leads to an increase in transmitter release (glutamate) at their synapses and consequent depolarization of the on-center ganglion cells that they contact via AMPA, kainite, and NMDA receptors. The selective response of on- and off- center bipolar cells to light increments and decre- ments is explained by the fact that they express different types of glutamate receptors. Off-center bipolar cells have ionotropic receptors (AMPA and kainate) that cause the cells to depolarize in response to glutamate released from photorecep- tor terminals. In contrast, on-center bipolar cells express a G-protein-coupled metabotropic gluta- mate receptor (mGluR6). When bound to gluta- mate, these receptors activate an intracellular cascade that closes cGMP-gated Na+ channels, reducing inward current and hyperpolarizing the cell. Decrements in light intensity naturally have the opposite effect on these two classes of bipolar cells, hyperpolarizing on-center cells and depolarizing off-center ones. Retinal ganglion cells are relatively poor at signaling differences in the level of diffuse illumination. Instead, they are sensitive to differences between the level of
illumination that falls on the receptive field center and the level of illumination that falls on the sur- round—that is, to luminance contrast. The center of a ganglion cell receptive field is surrounded by a concentric region (surround) that, when stimu- lated, antagonizes the response to stimulation of the receptive field center (center antagonism). In practice this means that firing of an on-center ganglion cell is (i) increased above baseline when a spot of light shines on receptive field center, (ii) at baseline when the spot of light is on the center/ surround border or outside of the receptive field completely, and (iii) reduced below baseline when shined on the surround alone. Off-center gan- glion cells demonstrate surround antagonism. Much of the antagonism is thought to arise via lateral connections established by horizontal cells and photoreceptor terminals (lateral inhibition). Thus, the information supplied by the retina to central visual stations for further processing does not give equal weight to all regions of the visual scene; rather, it emphasizes the regions where there are differences in luminance. In addition to making ganglion cells especially sensitive to light-dark borders in the visual scene, center- surround mechanisms make a significant contri- bution to the process of light adaptation as back- ground/ambient level of illumination is less important than scaled differences in light inten- sity. (In Chapter 10 Visual System In: Purves D, et al. (Eds.) Neuroscience 3rd ed. MA: Sinauer.)

Question 25

Which one of the following statements about
olfaction is LEAST accurate?
a. Bowman glands secrete a fluid that bathes the cilia of the receptors and acts as a solvent for odorant molecules
b. Mucus-coated olfactory epithelium lines the anterodorsal parts of the nasal cavities
c. Binding of odor molecules generates action potentials in a G-protein coupled mechanism
d. Fibers of CN I synapse with the mitral cells of the olfactory bulb
e. Olfactory tract and lateral olfactory stria project to the primary olfactory cortex and amygdala

Answer 25

b. Mucus-coated olfactory epithelium lines the anterodorsal parts of the nasal cavities

Smell is detected by olfactory receptor cells, which are situated in mucus-coated olfactory epithelium that lines the posterodorsal parts of the nasal cavities. Olfactory glands (Bowman glands) secrete a fluid that bathes the cilia of the receptors and acts as a solvent for odorant molecules. Olfactory receptor cells (first-order neurons) are stimulated by the binding of odor molecules to their cilia—G protein activation and activation of adenylyl cyclase, a rise in intra- cellular cAMP with causes opening of a cyclic- nucleotide gated ion channel allowing influx of Na+ and Ca2+ causing neuronal depolarization. The axons of the olfactory receptor cells form CN I (olfactory nerve); these project through the cribriform plate at the base of the cranium to synapse with the mitral cells of the olfactory bulb in olfactory glomeruli. The map of glomerular activation patterns within the olfactory bulb are thought to represent the quality of the odor being detected. The mitral cells of the olfactory bulb are excitatory, second-order neurons. The output axons of the mitral cells form the olfactory tract and lateral olfactory stria, both of which project to the primary olfactory cortex (prefrontal cortex) and the amygdala.

Question 26

Which one of the following statements
regarding taste sensation is LEAST accurate?
a. Receptors for molecules associated with
sweet and bitter tastes utilize second
messengers
b. Sour and salty-tasting molecules act directly upon the ion channels
c. Taste buds on the anterior two thirds of the tongue sendsignals through the lingual nerve to the chorda tympani and finally into CN VII (facial)
d. Posterior one-third of the tongue detects bitter and sour tastes and signal through
glossopharyngeal and vagus nerves
e. All taste fibers synapse in the nucleus ambiguus

Answer 26

e. All taste fibers synapse in the nucleus ambiguus

Taste is detected by taste receptor cells, which are located on specialized papillae of the taste buds and are stimulated by taste chemicals. The cellu- lar mechanism for transduction of taste stimuli depends upon the stimulus. Receptors for mole- cules associated with sweet and bitter tastes utilize second messengers, while those associated with sour and salty-tasting molecules act directly upon the ion channels. Taste buds on the anterior two thirds of the tongue have fungiform papillae and primarily detect sweet and salty tastes. They send signals centrally through the lingual nerve to the chorda tympani and finally into CN VII (facial). Taste buds on the posterior one third of the tongue have circumvallate papillae and foliate papillae, which detect bitter and sour tastes. Most of them send signals centrally through CN IX (glossopharyngeal); however, some located in the back of the throat and epiglottis send signals centrally through CN X (vagus). CN VII, IX, and X synapse with the tractus solitarius (solitary nucleus). Second-order neurons leave the solitary nucleus and project ipsilaterally to the ventral posterior medial nucleus of the thalamus. Neurons from the thalamus project to the taste cortex located in the primary somatosensory cortex. Taste discrimination and perception occur as a result of the comparison of the activation pattern of different groups of taste fibers.

Question 27

Which one of the following statements concerning neurotransmission at the neuromuscular junction is most accurate?
a. It is dependent upon the release of norepinephrine from the nerve ending
b. End plate potential amplitude can be much larger than that of excitatory or inhibitory postsynaptic potentials
c. It is an all-or-none response
d. It is not directly related to the concentration of transmitter released from the pre-
synaptic terminals
e. It is dependent on the opening of ligandgated calcium channels

Answer 27

b. End plate potential amplitude can be much larger than that of excitatory or inhibitory postsynaptic potentials

An action potential in presynaptic neuron causes calcium influx and release of acetylcho- line (ACh) from presynaptic vesicles stored in terminal bouton. Diffusion of ACh occurs across the synaptic cleft and it binds to postsyn- aptic nicotinic ACh receptors which are ligand- gated ion channels selective for Na+ and K+ ions, with subsequent current flow producing membrane depolarization (end-plate potential, EPP). The EPP is a graded potential (rather than an all-or-none response) with an ampli- tude directly related to the quantity of neurotransmitter (ACh) released from the pre- synaptic terminals. The amplitude of the EPP can be much greater that of the excitatory and inhibitory postsynaptic potentials in CNS syn- apses. At the neuromuscular junction, ACh is enzymatically degraded by acetylcholinesterase into acetate and choline. Choline is then taken up by the presynaptic terminal.

Question 28

Which one of the following statements regarding peripheral nerve injury is most accurate?
a. Neuropraxia involves disruption of the
myelin sheath only with some evidence
of Wallerian degeneration
b. Recovery after neuropraxia is likely to be incomplete
c. Neurotmesis is ideally managed with expectant management
d. Axonotmesis shows Wallerian degeneration distal to injury
e. A dense motor and sensory deficit following a penetrating injury is due to
neuropraxia

Answer 28

d. Axonotmesis shows Wallerian degeneration distal to injury

At times, it is difficult to tell what form of injury a patient has sustained. Certainly, if a patient has a dense motor and sensory deficit following a penetrating injury, it probably represents a neurotmesis and the patient will benefit from an exploration and nerve repair. On the other hand, if a patient sustained blunt trauma to the upper extremity and now has a partial sensory and motor deficit, it is difficult to know what form of nerve injury they have sustained. Exploration of this wound may not be indicated imme- diately following the injury and the wait-and-see approach may be more appropriate. Surgical repair may involve end-to-end neurorrhaphy (either epineural repair or fascicular repair with cable nerve grafts), nerve graft reconstruction of peripheral nerve (using donor nerves), neural conduit (e.g., if significant peripheral nerve gap) and less frequently, end-to-side neurorrhaphy.

Question 29

Which one of the following ensures sufficient
contraction of the striated portion of intrafusal fibers to enable monitor changes in muscle length?
a. Unmyelinated C fibers
b. 1A fibers
c. Gamma motor neurons
d. Alpha motor neurons
e. General visceral efferent fibers

Answer 29

c. Gamma motor neurons

Neuromuscular spindles are stretch receptor organs within skeletal muscles which are respon- sible for the regulation of muscle tone via the spinal stretch reflex. They lie parallel to the mus- cle fibers, embedded in endomysium or perimy- sium. Each spindle contains 2-10 modified skeletal muscle fibers called intrafusal fibers, which are much smaller than skeletal extrafusal fibers. The intrafusal fibers have a central non- striated area in which their nuclei tend to be con- centrated. The two types of intrafusal fibers are nuclear bag fiber and nuclear chain fiber. Asso- ciated with the intrafusal fibers are branched non-myelinated endings of large myelinated sen- sory fibers which wrap around the central non- striated area, forming annulospiral endings. Additionally, flower-spray endings of smaller myelinated sensory nerves are located on the striated portions of the intrafusal fibers. These sensory receptors are stimulated by stretching of the intrafusal fibers, which occurs when the (extrafusal) muscle mass is stretched. This stim- ulus evokes a simple two-neuron spinal cord reflex, causing contraction of the extrafusal mus- cle mass. This removes the stretch stimulus from the spindle and equilibrium is restored (e.g., knee jerk reflex). The sensitivity of the neuro- muscular spindle to stretch is modulated via small gamma motor neurons controlled by the extra-pyramidal motor system. These gamma motor neurons innervate the striated portions of the intrafusal fibers; contraction of the intra- fusal fibers increases the stretch on the fibers and thus the sensitivity of the receptors to stretching of the extrafusal muscle mass. During a normal movement, both alpha and gamma motor neu- rons are co-activated. If only the alpha motor neurons were activated the muscle would con- tract and the central non-contractile portion of intrafusal muscle fibers would become slack
and unable to monitor changes in muscle length. However, where descending inhibition on gamma motor neurons is impaired (e.g., UMN lesion), this can result in exquisitely sensitive stretch receptors and hyperreflexia.