STAHL'S ESSENTIAL PSYCHOPHARMACOLOGY
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1)
Reference: Ch. 1 — Chemical Neurotransmission —
Neurotransmitter Release & Vesicular Storage
Stem: A 34-year-old woman with major depressive disorder
failed two prior antidepressant trials (an SSRI and an SNRI) and
now reports persistent anhedonia despite improved mood. She
has minimal insomnia and no psychomotor agitation. You are
considering augmenting with a medication that increases
presynaptic monoamine availability by inhibiting vesicular
uptake. Which mechanism is most consistent with that
strategy?
,A. Inhibition of the vesicular monoamine transporter (VMAT2)
to prevent monoamine vesicular loading.
B. Blockade of monoamine oxidase (MAO) to reduce
intracellular catabolism.
C. Inhibition of plasma membrane monoamine transporters
(SERT/DAT/NET) to reduce reuptake.
D. Potentiation of postsynaptic receptor sensitivity via positive
allosteric modulation.
Correct answer: B
Rationale — Correct (B): Inhibiting MAO reduces intracellular
breakdown of monoamines, increasing cytosolic monoamine
available for vesicular refilling and release. Stahl describes MAO
inhibition as increasing presynaptic monoamine pools and
facilitating transmitter release, which can restore hedonic
circuitry when reuptake blockade alone is insufficient. This
aligns with augmenting presynaptic availability rather than
blocking vesicular uptake.
Rationale — Incorrect:
A: VMAT2 inhibition decreases vesicular storage and reduces
synaptic release — the opposite of the clinical goal.
C: Reuptake inhibition (SERT/DAT/NET) increases synaptic
concentrations but does not directly increase presynaptic
cytosolic pools the way MAO inhibition does.
D: Positive allosteric modulation of postsynaptic receptors
enhances receptor response but does not increase presynaptic
monoamine availability.
,Teaching point: MAO inhibition raises presynaptic monoamine
pools by reducing intracellular catabolism.
Citation: Stahl, S. M. (2021). Essential Psychopharmacology (5th
ed.). Ch. 1.
2)
Reference: Ch. 1 — Chemical Neurotransmission —
Autoreceptors and Feedback Regulation
Stem: A 45-year-old man began an SSRI for generalized anxiety
disorder and reports increased anxiety and restlessness during
the first three weeks of treatment. His psychiatrist explains this
may reflect an early autoreceptor effect. Which autoreceptor
mechanism best explains transient SSRI-associated activation?
A. Postsynaptic receptor up-regulation increasing excitatory
drive.
B. Presynaptic 5-HT1A autoreceptor activation reducing
serotonin release.
C. Heteroreceptor blockade on GABAergic interneurons
increasing inhibition.
D. Rapid down-regulation of presynaptic autoreceptors causing
initial decreased release.
Correct answer: B
Rationale — Correct (B): Stahl outlines that initial SSRI-induced
increases in synaptic serotonin stimulate presynaptic 5-HT1A
autoreceptors, which suppress further serotonin release,
, sometimes producing transient anxiety/activation. Over weeks,
desensitization of these autoreceptors permits increased
serotonergic neurotransmission and symptomatic
improvement.
Rationale — Incorrect:
A: Postsynaptic up-regulation is not the initial mechanism
causing early activation.
C: Heteroreceptor blockade on GABAergic interneurons would
increase inhibition, opposing activation.
D: Rapid down-regulation of autoreceptors produces increased
release later, not the early reduction that causes activation.
Teaching point: Early SSRI activation often reflects 5-HT1A
autoreceptor-mediated inhibition of serotonin release.
Citation: Stahl, S. M. (2021). Essential Psychopharmacology (5th
ed.). Ch. 1.
3)
Reference: Ch. 1 — Chemical Neurotransmission — Ionotropic
vs Metabotropic Receptors
Stem: A 28-year-old male with bipolar II experiences acute
anxiety and agitation; you plan a rapid anxiolytic with short
latency of effect. According to receptor kinetics described in
Stahl Chapter 1, which receptor target would most reliably
produce the fastest clinical anxiolysis?
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1)
Reference: Ch. 1 — Chemical Neurotransmission —
Neurotransmitter Release & Vesicular Storage
Stem: A 34-year-old woman with major depressive disorder
failed two prior antidepressant trials (an SSRI and an SNRI) and
now reports persistent anhedonia despite improved mood. She
has minimal insomnia and no psychomotor agitation. You are
considering augmenting with a medication that increases
presynaptic monoamine availability by inhibiting vesicular
uptake. Which mechanism is most consistent with that
strategy?
,A. Inhibition of the vesicular monoamine transporter (VMAT2)
to prevent monoamine vesicular loading.
B. Blockade of monoamine oxidase (MAO) to reduce
intracellular catabolism.
C. Inhibition of plasma membrane monoamine transporters
(SERT/DAT/NET) to reduce reuptake.
D. Potentiation of postsynaptic receptor sensitivity via positive
allosteric modulation.
Correct answer: B
Rationale — Correct (B): Inhibiting MAO reduces intracellular
breakdown of monoamines, increasing cytosolic monoamine
available for vesicular refilling and release. Stahl describes MAO
inhibition as increasing presynaptic monoamine pools and
facilitating transmitter release, which can restore hedonic
circuitry when reuptake blockade alone is insufficient. This
aligns with augmenting presynaptic availability rather than
blocking vesicular uptake.
Rationale — Incorrect:
A: VMAT2 inhibition decreases vesicular storage and reduces
synaptic release — the opposite of the clinical goal.
C: Reuptake inhibition (SERT/DAT/NET) increases synaptic
concentrations but does not directly increase presynaptic
cytosolic pools the way MAO inhibition does.
D: Positive allosteric modulation of postsynaptic receptors
enhances receptor response but does not increase presynaptic
monoamine availability.
,Teaching point: MAO inhibition raises presynaptic monoamine
pools by reducing intracellular catabolism.
Citation: Stahl, S. M. (2021). Essential Psychopharmacology (5th
ed.). Ch. 1.
2)
Reference: Ch. 1 — Chemical Neurotransmission —
Autoreceptors and Feedback Regulation
Stem: A 45-year-old man began an SSRI for generalized anxiety
disorder and reports increased anxiety and restlessness during
the first three weeks of treatment. His psychiatrist explains this
may reflect an early autoreceptor effect. Which autoreceptor
mechanism best explains transient SSRI-associated activation?
A. Postsynaptic receptor up-regulation increasing excitatory
drive.
B. Presynaptic 5-HT1A autoreceptor activation reducing
serotonin release.
C. Heteroreceptor blockade on GABAergic interneurons
increasing inhibition.
D. Rapid down-regulation of presynaptic autoreceptors causing
initial decreased release.
Correct answer: B
Rationale — Correct (B): Stahl outlines that initial SSRI-induced
increases in synaptic serotonin stimulate presynaptic 5-HT1A
autoreceptors, which suppress further serotonin release,
, sometimes producing transient anxiety/activation. Over weeks,
desensitization of these autoreceptors permits increased
serotonergic neurotransmission and symptomatic
improvement.
Rationale — Incorrect:
A: Postsynaptic up-regulation is not the initial mechanism
causing early activation.
C: Heteroreceptor blockade on GABAergic interneurons would
increase inhibition, opposing activation.
D: Rapid down-regulation of autoreceptors produces increased
release later, not the early reduction that causes activation.
Teaching point: Early SSRI activation often reflects 5-HT1A
autoreceptor-mediated inhibition of serotonin release.
Citation: Stahl, S. M. (2021). Essential Psychopharmacology (5th
ed.). Ch. 1.
3)
Reference: Ch. 1 — Chemical Neurotransmission — Ionotropic
vs Metabotropic Receptors
Stem: A 28-year-old male with bipolar II experiences acute
anxiety and agitation; you plan a rapid anxiolytic with short
latency of effect. According to receptor kinetics described in
Stahl Chapter 1, which receptor target would most reliably
produce the fastest clinical anxiolysis?
