Stahl's Essential Psychopharmacology
Neuroscientific Basis and Practical Applications
5th Edition
Author(s)Stephen M. Stahl
TEST BANK
Item 1
Reference: Ch. 1, Chemical Neurotransmission — Presynaptic
mechanisms / Neurotransmitter release
Question Stem: A patient is taking a medication that blocks
voltage-gated calcium channels in presynaptic terminals. Which
immediate effect on synaptic transmission is most likely?
A. Increased quantal size from individual vesicles
B. Reduced probability of neurotransmitter release (reduced
vesicle exocytosis)
C. Increased reuptake of released neurotransmitter by
transporters
D. Upregulation of postsynaptic receptor density within minutes
Correct Answer: B
Rationales:
, • Correct (B): Blocking presynaptic voltage-gated calcium
channels decreases Ca²⁺ influx required for vesicle fusion,
lowering the probability of neurotransmitter release. This
is the primary acute effect on synaptic transmission.
• A: Quantal size (amount released per vesicle) is not
increased by reducing Ca²⁺ influx—if anything, fewer
vesicles fuse.
• C: Reuptake transporters operate on released transmitter;
blocking Ca²⁺ channels reduces release rather than
increasing transporter activity.
• D: Postsynaptic receptor density changes
(trafficking/upregulation) typically occur over hours–days,
not immediately within minutes.
Teaching Point: Presynaptic Ca²⁺ entry is essential for vesicle
exocytosis and release probability.
Citation: Ch. 1, Chemical Neurotransmission — Presynaptic
mechanisms / Neurotransmitter release.
Item 2
Reference: Ch. 1, Chemical Neurotransmission — Vesicle cycle &
storage
Question Stem: A new drug selectively inhibits the vesicular
monoamine transporter (VMAT2). Which clinical pharmacologic
effect is most consistent with VMAT2 inhibition?
,A. Increased synaptic dopamine and norepinephrine
concentration
B. Depletion of monoamines from presynaptic terminals and
reduced neurotransmission
C. Selective blockade of postsynaptic monoamine receptors
D. Enhanced synthesis of monoamines through upregulated
rate-limiting enzymes
Correct Answer: B
Rationales:
• Correct (B): VMAT2 loads monoamines into synaptic
vesicles for storage; inhibition prevents vesicular storage
causing cytosolic degradation and depletion of released
monoamines, reducing neurotransmission.
• A: Inhibiting VMAT2 does not increase synaptic
monoamines; it reduces vesicular release.
• C: VMAT2 inhibitors act presynaptically on vesicle loading,
not by blocking postsynaptic receptors.
• D: VMAT2 inhibition does not directly increase synthetic
enzyme activity; synthesis may be downregulated with
depleted vesicular stores.
Teaching Point: VMAT2 inhibition depletes vesicular
monoamines and reduces synaptic release.
Citation: Ch. 1, Chemical Neurotransmission — Vesicle cycle &
storage.
, Item 3
Reference: Ch. 1, Chemical Neurotransmission —
Neurotransmitter synthesis & metabolic pathways
Question Stem: A patient treated with an MAO inhibitor
develops hypertensive crisis after ingesting tyramine-rich food.
Which mechanism best explains this reaction?
A. MAO inhibition prevents tyramine deamination in the gut
and nerve terminals leading to increased noradrenergic release.
B. MAO inhibition increases postsynaptic α₂-autoreceptor
sensitivity causing vasoconstriction.
C. MAO inhibitors block monoamine reuptake transporters,
directly increasing synaptic norepinephrine.
D. Tyramine is converted to serotonin when MAO is inhibited,
causing vasospasm.
Correct Answer: A
Rationales:
• Correct (A): MAO normally degrades dietary tyramine and
intraneuronal monoamines; MAO inhibition allows
tyramine to enter sympathetic terminals and trigger
release of stored norepinephrine, causing hypertensive
crisis.
• B: α₂-autoreceptor hypersensitivity is not the mechanism
for acute tyramine-induced hypertensive crises.
Neuroscientific Basis and Practical Applications
5th Edition
Author(s)Stephen M. Stahl
TEST BANK
Item 1
Reference: Ch. 1, Chemical Neurotransmission — Presynaptic
mechanisms / Neurotransmitter release
Question Stem: A patient is taking a medication that blocks
voltage-gated calcium channels in presynaptic terminals. Which
immediate effect on synaptic transmission is most likely?
A. Increased quantal size from individual vesicles
B. Reduced probability of neurotransmitter release (reduced
vesicle exocytosis)
C. Increased reuptake of released neurotransmitter by
transporters
D. Upregulation of postsynaptic receptor density within minutes
Correct Answer: B
Rationales:
, • Correct (B): Blocking presynaptic voltage-gated calcium
channels decreases Ca²⁺ influx required for vesicle fusion,
lowering the probability of neurotransmitter release. This
is the primary acute effect on synaptic transmission.
• A: Quantal size (amount released per vesicle) is not
increased by reducing Ca²⁺ influx—if anything, fewer
vesicles fuse.
• C: Reuptake transporters operate on released transmitter;
blocking Ca²⁺ channels reduces release rather than
increasing transporter activity.
• D: Postsynaptic receptor density changes
(trafficking/upregulation) typically occur over hours–days,
not immediately within minutes.
Teaching Point: Presynaptic Ca²⁺ entry is essential for vesicle
exocytosis and release probability.
Citation: Ch. 1, Chemical Neurotransmission — Presynaptic
mechanisms / Neurotransmitter release.
Item 2
Reference: Ch. 1, Chemical Neurotransmission — Vesicle cycle &
storage
Question Stem: A new drug selectively inhibits the vesicular
monoamine transporter (VMAT2). Which clinical pharmacologic
effect is most consistent with VMAT2 inhibition?
,A. Increased synaptic dopamine and norepinephrine
concentration
B. Depletion of monoamines from presynaptic terminals and
reduced neurotransmission
C. Selective blockade of postsynaptic monoamine receptors
D. Enhanced synthesis of monoamines through upregulated
rate-limiting enzymes
Correct Answer: B
Rationales:
• Correct (B): VMAT2 loads monoamines into synaptic
vesicles for storage; inhibition prevents vesicular storage
causing cytosolic degradation and depletion of released
monoamines, reducing neurotransmission.
• A: Inhibiting VMAT2 does not increase synaptic
monoamines; it reduces vesicular release.
• C: VMAT2 inhibitors act presynaptically on vesicle loading,
not by blocking postsynaptic receptors.
• D: VMAT2 inhibition does not directly increase synthetic
enzyme activity; synthesis may be downregulated with
depleted vesicular stores.
Teaching Point: VMAT2 inhibition depletes vesicular
monoamines and reduces synaptic release.
Citation: Ch. 1, Chemical Neurotransmission — Vesicle cycle &
storage.
, Item 3
Reference: Ch. 1, Chemical Neurotransmission —
Neurotransmitter synthesis & metabolic pathways
Question Stem: A patient treated with an MAO inhibitor
develops hypertensive crisis after ingesting tyramine-rich food.
Which mechanism best explains this reaction?
A. MAO inhibition prevents tyramine deamination in the gut
and nerve terminals leading to increased noradrenergic release.
B. MAO inhibition increases postsynaptic α₂-autoreceptor
sensitivity causing vasoconstriction.
C. MAO inhibitors block monoamine reuptake transporters,
directly increasing synaptic norepinephrine.
D. Tyramine is converted to serotonin when MAO is inhibited,
causing vasospasm.
Correct Answer: A
Rationales:
• Correct (A): MAO normally degrades dietary tyramine and
intraneuronal monoamines; MAO inhibition allows
tyramine to enter sympathetic terminals and trigger
release of stored norepinephrine, causing hypertensive
crisis.
• B: α₂-autoreceptor hypersensitivity is not the mechanism
for acute tyramine-induced hypertensive crises.
