STAHL'S ESSENTIAL PSYCHOPHARMACOLOGY
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1️⃣
Reference
Ch. 1 — Chemical Neurotransmission — Vesicular packaging &
release
Stem
A 32-year-old patient with chronic major depressive disorder
reports poor response to an SSRI. You suspect presynaptic
monoamine availability is limiting therapeutic effect. Which
pharmacologic strategy most directly increases cytosolic
monoamine availability for vesicular packaging and activity-
dependent release?
A. Inhibit monoamine oxidase (MAO)
B. Block vesicular monoamine transporter (VMAT)
,C. Enhance monoamine reuptake transporter (increase SERT
function)
D. Potentiate postsynaptic receptor signaling with a positive
allosteric modulator
Correct Answer
A
Rationales
Correct (A): MAO inhibition reduces intraneuronal enzymatic
breakdown of monoamines, increasing cytosolic monoamine
levels available for vesicular uptake via VMAT and subsequent
release. Stahl describes MAO as the principal degradative
pathway—blocking it raises presynaptic stores.
Incorrect (B): Blocking VMAT would decrease vesicular
packaging and deplete releasable monoamines, worsening
availability.
Incorrect (C): Increasing SERT function would increase reuptake
from the synapse into the cytosol but does not prevent
enzymatic degradation; net effect on releasable vesicular stores
is not a targeted way to increase availability.
Incorrect (D): Potentiating postsynaptic signaling does not
increase presynaptic monoamine stores or vesicular release.
Teaching Point
MAO inhibition increases presynaptic monoamine availability
for vesicular packaging and release.
,Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2️⃣
Reference
Ch. 1 — Chemical Neurotransmission — VMAT and drug effects
Stem
A patient with Parkinsonian tremor is treated with a medication
that depletes presynaptic monoamines and develops worsening
depression. Which mechanism best explains medication-
induced mood worsening?
A. VMAT inhibition → reduced vesicular monoamine storage
and release
B. SERT inhibition → increased synaptic serotonin and improved
mood
C. Postsynaptic receptor antagonism → increased downstream
signaling
D. GABAergic potentiation → increased monoamine release
Correct Answer
A
Rationales
Correct (A): VMAT inhibition reduces vesicular storage of
monoamines, causing presynaptic depletion and reduced
synaptic release—consistent with drug-induced depressive
, symptoms. Stahl notes VMAT function as essential for
maintaining releasable pools.
Incorrect (B): SERT inhibition raises synaptic serotonin, typically
antidepressant rather than depressive.
Incorrect (C): Postsynaptic receptor antagonism generally
decreases downstream signaling; it would not explain
presynaptic monoamine depletion.
Incorrect (D): GABAergic potentiation suppresses excitatory
firing and would not increase monoamine release in this
context.
Teaching Point
VMAT function is necessary to maintain releasable monoamine
pools; VMAT blockade causes depletion and depressive effects.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
3️⃣
Reference
Ch. 1 — Chemical Neurotransmission — Reuptake transporters
& kinetics
Stem
A 45-year-old with panic disorder has partial symptom relief
with an SSRI. You consider switching to an SNRI.
Mechanistically, how would SNRI action alter synaptic
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1️⃣
Reference
Ch. 1 — Chemical Neurotransmission — Vesicular packaging &
release
Stem
A 32-year-old patient with chronic major depressive disorder
reports poor response to an SSRI. You suspect presynaptic
monoamine availability is limiting therapeutic effect. Which
pharmacologic strategy most directly increases cytosolic
monoamine availability for vesicular packaging and activity-
dependent release?
A. Inhibit monoamine oxidase (MAO)
B. Block vesicular monoamine transporter (VMAT)
,C. Enhance monoamine reuptake transporter (increase SERT
function)
D. Potentiate postsynaptic receptor signaling with a positive
allosteric modulator
Correct Answer
A
Rationales
Correct (A): MAO inhibition reduces intraneuronal enzymatic
breakdown of monoamines, increasing cytosolic monoamine
levels available for vesicular uptake via VMAT and subsequent
release. Stahl describes MAO as the principal degradative
pathway—blocking it raises presynaptic stores.
Incorrect (B): Blocking VMAT would decrease vesicular
packaging and deplete releasable monoamines, worsening
availability.
Incorrect (C): Increasing SERT function would increase reuptake
from the synapse into the cytosol but does not prevent
enzymatic degradation; net effect on releasable vesicular stores
is not a targeted way to increase availability.
Incorrect (D): Potentiating postsynaptic signaling does not
increase presynaptic monoamine stores or vesicular release.
Teaching Point
MAO inhibition increases presynaptic monoamine availability
for vesicular packaging and release.
,Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2️⃣
Reference
Ch. 1 — Chemical Neurotransmission — VMAT and drug effects
Stem
A patient with Parkinsonian tremor is treated with a medication
that depletes presynaptic monoamines and develops worsening
depression. Which mechanism best explains medication-
induced mood worsening?
A. VMAT inhibition → reduced vesicular monoamine storage
and release
B. SERT inhibition → increased synaptic serotonin and improved
mood
C. Postsynaptic receptor antagonism → increased downstream
signaling
D. GABAergic potentiation → increased monoamine release
Correct Answer
A
Rationales
Correct (A): VMAT inhibition reduces vesicular storage of
monoamines, causing presynaptic depletion and reduced
synaptic release—consistent with drug-induced depressive
, symptoms. Stahl notes VMAT function as essential for
maintaining releasable pools.
Incorrect (B): SERT inhibition raises synaptic serotonin, typically
antidepressant rather than depressive.
Incorrect (C): Postsynaptic receptor antagonism generally
decreases downstream signaling; it would not explain
presynaptic monoamine depletion.
Incorrect (D): GABAergic potentiation suppresses excitatory
firing and would not increase monoamine release in this
context.
Teaching Point
VMAT function is necessary to maintain releasable monoamine
pools; VMAT blockade causes depletion and depressive effects.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
3️⃣
Reference
Ch. 1 — Chemical Neurotransmission — Reuptake transporters
& kinetics
Stem
A 45-year-old with panic disorder has partial symptom relief
with an SSRI. You consider switching to an SNRI.
Mechanistically, how would SNRI action alter synaptic
