STAHL'S ESSENTIAL PSYCHOPHARMACOLOGY
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission — Vesicular storage &
release
Stem
A 34-year-old patient with treatment-resistant depressive
symptoms reports partial benefit from an SSRI but now has
worsening fatigue and orthostatic lightheadedness. You
consider switching to a drug that enhances synaptic
monoamine availability by increasing vesicular release rather
than blocking reuptake. Which pharmacologic strategy best
matches this mechanism described in Stahl Ch. 1?
,Options
A. Inhibit vesicular monoamine transporter (VMAT) to deplete
presynaptic stores.
B. Enhance vesicular filling via VMAT modulation to increase
quantal release.
C. Block presynaptic monoamine reuptake transporters.
D. Irreversibly inhibit monoamine oxidase in the cytosol.
Correct answer
B
Rationales
Correct (B) — Stahl describes that increasing vesicular filling
increases quantal release and synaptic availability; a drug that
enhances VMAT-mediated vesicular uptake or promotes vesicle
release increases transmitter release without primarily relying
on reuptake blockade. This matches the vignette goal to boost
synaptic monoamines through vesicular mechanisms rather
than reuptake inhibition.
Incorrect (A) — VMAT inhibition reduces vesicular storage,
depleting synaptic monoamines and worsening mood, opposite
the intended effect.
Incorrect (C) — Reuptake blockade increases synaptic levels by
preventing clearance, but the stem specifies a vesicular-release
strategy rather than transporter inhibition.
Incorrect (D) — MAO inhibition reduces enzymatic breakdown
and increases cytosolic monoamines but does not specifically
enhance vesicular quantal release as described.
,Teaching Point
Enhancing vesicular filling increases quantal neurotransmitter
release; VMAT directionality matters.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission — Reuptake transporters
& kinetics
Stem
A 45-year-old patient with generalized anxiety disorder is
sensitive to activation side effects (restlessness, insomnia) with
SNRIs. You consider a medication strategy that retains
serotonergic tone while reducing phasic increases in synaptic
norepinephrine caused by transporter blockade. Based on
transporter kinetics in Stahl Ch. 1, which option is most
consistent?
Options
A. Use a high-affinity NET inhibitor with fast on-off kinetics.
B. Use a low-affinity NET inhibitor with slow dissociation (long
dwell time).
C. Prefer a selective serotonin reuptake inhibitor (SSRI) without
NET inhibition.
, D. Combine NET inhibitor with a presynaptic α2 agonist to
dampen NE release.
Correct answer
C
Rationales
Correct (C) — Stahl emphasizes transporter selectivity: avoiding
NET blockade minimizes phasic NE increases associated with
activation. Choosing an SSRI preserves serotonergic tone while
reducing norepinephrine-driven activation risks.
Incorrect (A) — High-affinity NET inhibition, even with fast
kinetics, still produces NET blockade and risks NE-related
activation.
Incorrect (B) — Low-affinity with long dwell time would
produce more sustained NET blockade and likely more
activation.
Incorrect (D) — Combining NET inhibition with an α2 agonist
could blunt NE release but introduces additional
pharmacodynamic complexity and side effects; the simplest
mechanism-consistent choice is to avoid NET action.
Teaching Point
Transporter selectivity determines activation risk; avoid NET
activity to reduce noradrenergic stimulation.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission — Vesicular storage &
release
Stem
A 34-year-old patient with treatment-resistant depressive
symptoms reports partial benefit from an SSRI but now has
worsening fatigue and orthostatic lightheadedness. You
consider switching to a drug that enhances synaptic
monoamine availability by increasing vesicular release rather
than blocking reuptake. Which pharmacologic strategy best
matches this mechanism described in Stahl Ch. 1?
,Options
A. Inhibit vesicular monoamine transporter (VMAT) to deplete
presynaptic stores.
B. Enhance vesicular filling via VMAT modulation to increase
quantal release.
C. Block presynaptic monoamine reuptake transporters.
D. Irreversibly inhibit monoamine oxidase in the cytosol.
Correct answer
B
Rationales
Correct (B) — Stahl describes that increasing vesicular filling
increases quantal release and synaptic availability; a drug that
enhances VMAT-mediated vesicular uptake or promotes vesicle
release increases transmitter release without primarily relying
on reuptake blockade. This matches the vignette goal to boost
synaptic monoamines through vesicular mechanisms rather
than reuptake inhibition.
Incorrect (A) — VMAT inhibition reduces vesicular storage,
depleting synaptic monoamines and worsening mood, opposite
the intended effect.
Incorrect (C) — Reuptake blockade increases synaptic levels by
preventing clearance, but the stem specifies a vesicular-release
strategy rather than transporter inhibition.
Incorrect (D) — MAO inhibition reduces enzymatic breakdown
and increases cytosolic monoamines but does not specifically
enhance vesicular quantal release as described.
,Teaching Point
Enhancing vesicular filling increases quantal neurotransmitter
release; VMAT directionality matters.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission — Reuptake transporters
& kinetics
Stem
A 45-year-old patient with generalized anxiety disorder is
sensitive to activation side effects (restlessness, insomnia) with
SNRIs. You consider a medication strategy that retains
serotonergic tone while reducing phasic increases in synaptic
norepinephrine caused by transporter blockade. Based on
transporter kinetics in Stahl Ch. 1, which option is most
consistent?
Options
A. Use a high-affinity NET inhibitor with fast on-off kinetics.
B. Use a low-affinity NET inhibitor with slow dissociation (long
dwell time).
C. Prefer a selective serotonin reuptake inhibitor (SSRI) without
NET inhibition.
, D. Combine NET inhibitor with a presynaptic α2 agonist to
dampen NE release.
Correct answer
C
Rationales
Correct (C) — Stahl emphasizes transporter selectivity: avoiding
NET blockade minimizes phasic NE increases associated with
activation. Choosing an SSRI preserves serotonergic tone while
reducing norepinephrine-driven activation risks.
Incorrect (A) — High-affinity NET inhibition, even with fast
kinetics, still produces NET blockade and risks NE-related
activation.
Incorrect (B) — Low-affinity with long dwell time would
produce more sustained NET blockade and likely more
activation.
Incorrect (D) — Combining NET inhibition with an α2 agonist
could blunt NE release but introduces additional
pharmacodynamic complexity and side effects; the simplest
mechanism-consistent choice is to avoid NET action.
Teaching Point
Transporter selectivity determines activation risk; avoid NET
activity to reduce noradrenergic stimulation.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
