STAHL'S ESSENTIAL PSYCHOPHARMACOLOGY
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission
PMHNP-Level Question Stem (2–4 sentences)
A 48-year-old patient with treatment-resistant major depressive
disorder reports partial improvement with an SSRI but
persistent psychomotor retardation and low energy. They have
a history of poor adherence to complex dosing. Considering
presynaptic mechanisms and neurotransmitter availability,
which strategy best targets insufficient synaptic monoaminergic
tone while minimizing complexity and drug–drug interaction
risk?
,Options
A. Add a short-acting MAO inhibitor to increase intraneuronal
monoamine levels.
B. Switch to an antidepressant with norepinephrine transporter
(NET) inhibition that blocks presynaptic reuptake.
C. Augment with a postsynaptic receptor antagonist to increase
receptor sensitivity.
D. Add a monoamine releaser to force presynaptic release of
serotonin and norepinephrine.
Correct Answer
B
Rationales
Correct (B) — NET inhibition increases synaptic norepinephrine
(and often dopamine in certain projections) by blocking
reuptake, enhancing catecholaminergic neurotransmission
implicated in energy and psychomotor drive. Stahl emphasizes
targeting transporter-mediated reuptake to raise extracellular
monoamines without complex enzyme inhibition, which fits a
simpler regimen and lower interaction risk than MAO inhibition.
Incorrect (A) — MAO inhibitors raise intraneuronal and
extracellular monoamines broadly but carry significant dietary
and drug interaction risks and require complex monitoring; not
ideal for adherence concerns.
Incorrect (C) — A postsynaptic antagonist typically reduces
neurotransmission at that receptor and would not directly
address low synaptic monoamine availability; receptor
,antagonism is not a primary strategy to increase
monoaminergic tone.
Incorrect (D) — Monoamine releasers can non-selectively
release transmitters and produce sympathomimetic effects and
higher adverse-event risk; they are not first-line for treatment-
resistant depression in the context of safety/adherence
concerns.
Teaching Point (≤20 words)
Target transporters to safely raise synaptic monoamines; prefer
reuptake inhibition over MAO inhibition for simpler regimens.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission
PMHNP-Level Question Stem (2–4 sentences)
A 25-year-old with panic disorder experiences severe anxiety
spikes after starting an agent that increases synaptic serotonin
rapidly. Symptoms suggest possible serotonergic overactivation.
Which presynaptic or synaptic mechanism most plausibly
explains acute worsening of anxiety following abrupt elevation
of extracellular serotonin?
, Options
A. Desensitization of postsynaptic 5-HT2A receptors within
minutes.
B. Activation of somatodendritic 5-HT1A autoreceptors
producing transient decreases in serotonergic firing.
C. Immediate upregulation of serotonin transporter (SERT)
expression.
D. Increased vesicular monoamine transporter (VMAT) activity
causing amplified release.
Correct Answer
B
Rationales
Correct (B) — Elevated extracellular serotonin stimulates
somatodendritic 5-HT1A autoreceptors, which transiently
reduce serotonergic neuron firing and can paradoxically alter
downstream circuits and acute symptom expression; Stahl
discusses autoreceptor-mediated negative feedback as key to
early treatment effects.
Incorrect (A) — Receptor desensitization occurs over days to
weeks, not minutes; acute anxiety is more consistent with
autoreceptor or immediate receptor activation effects.
Incorrect (C) — SERT upregulation is not an immediate
compensatory response and would not explain acute symptom
worsening.
Incorrect (D) — VMAT increases would augment vesicular
storage/release over longer timeframes; immediate
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission
PMHNP-Level Question Stem (2–4 sentences)
A 48-year-old patient with treatment-resistant major depressive
disorder reports partial improvement with an SSRI but
persistent psychomotor retardation and low energy. They have
a history of poor adherence to complex dosing. Considering
presynaptic mechanisms and neurotransmitter availability,
which strategy best targets insufficient synaptic monoaminergic
tone while minimizing complexity and drug–drug interaction
risk?
,Options
A. Add a short-acting MAO inhibitor to increase intraneuronal
monoamine levels.
B. Switch to an antidepressant with norepinephrine transporter
(NET) inhibition that blocks presynaptic reuptake.
C. Augment with a postsynaptic receptor antagonist to increase
receptor sensitivity.
D. Add a monoamine releaser to force presynaptic release of
serotonin and norepinephrine.
Correct Answer
B
Rationales
Correct (B) — NET inhibition increases synaptic norepinephrine
(and often dopamine in certain projections) by blocking
reuptake, enhancing catecholaminergic neurotransmission
implicated in energy and psychomotor drive. Stahl emphasizes
targeting transporter-mediated reuptake to raise extracellular
monoamines without complex enzyme inhibition, which fits a
simpler regimen and lower interaction risk than MAO inhibition.
Incorrect (A) — MAO inhibitors raise intraneuronal and
extracellular monoamines broadly but carry significant dietary
and drug interaction risks and require complex monitoring; not
ideal for adherence concerns.
Incorrect (C) — A postsynaptic antagonist typically reduces
neurotransmission at that receptor and would not directly
address low synaptic monoamine availability; receptor
,antagonism is not a primary strategy to increase
monoaminergic tone.
Incorrect (D) — Monoamine releasers can non-selectively
release transmitters and produce sympathomimetic effects and
higher adverse-event risk; they are not first-line for treatment-
resistant depression in the context of safety/adherence
concerns.
Teaching Point (≤20 words)
Target transporters to safely raise synaptic monoamines; prefer
reuptake inhibition over MAO inhibition for simpler regimens.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission
PMHNP-Level Question Stem (2–4 sentences)
A 25-year-old with panic disorder experiences severe anxiety
spikes after starting an agent that increases synaptic serotonin
rapidly. Symptoms suggest possible serotonergic overactivation.
Which presynaptic or synaptic mechanism most plausibly
explains acute worsening of anxiety following abrupt elevation
of extracellular serotonin?
, Options
A. Desensitization of postsynaptic 5-HT2A receptors within
minutes.
B. Activation of somatodendritic 5-HT1A autoreceptors
producing transient decreases in serotonergic firing.
C. Immediate upregulation of serotonin transporter (SERT)
expression.
D. Increased vesicular monoamine transporter (VMAT) activity
causing amplified release.
Correct Answer
B
Rationales
Correct (B) — Elevated extracellular serotonin stimulates
somatodendritic 5-HT1A autoreceptors, which transiently
reduce serotonergic neuron firing and can paradoxically alter
downstream circuits and acute symptom expression; Stahl
discusses autoreceptor-mediated negative feedback as key to
early treatment effects.
Incorrect (A) — Receptor desensitization occurs over days to
weeks, not minutes; acute anxiety is more consistent with
autoreceptor or immediate receptor activation effects.
Incorrect (C) — SERT upregulation is not an immediate
compensatory response and would not explain acute symptom
worsening.
Incorrect (D) — VMAT increases would augment vesicular
storage/release over longer timeframes; immediate
