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 45-year-old patient with major depressive disorder reports
sudden episodes of increased anxiety and tremor shortly after
starting a high-dose tricyclic antidepressant (TCA). He also
reports dry mouth and constipation. Considering presynaptic
vesicular handling and anticholinergic/adrenergic effects, which
mechanism best explains the new tremor and autonomic
symptoms?
,Options
A. TCA blockade of vesicular monoamine transporter (VMAT2)
causing cytosolic monoamine depletion
B. TCA inhibition of monoamine reuptake transporters
increasing synaptic monoamines and anticholinergic
antagonism at muscarinic receptors
C. TCA activation of presynaptic α2-autoreceptors reducing
norepinephrine release
D. TCA agonism at postsynaptic GABA_A receptors causing
paradoxical excitation
Correct Answer
B
Rationales
• Correct (B): TCAs inhibit SERT and NET, increasing synaptic
monoamine levels which can provoke anxiety and tremor
through enhanced noradrenergic tone; TCAs also have
strong muscarinic antagonism explaining dry mouth and
constipation. Stahl emphasizes how transporter blockade
increases synaptic neurotransmitter availability producing
both therapeutic and noradrenergic/adrenergic side
effects.
• Incorrect (A): VMAT2 blockade reduces vesicular storage
(seen with tetrabenazine), causing parkinsonism and
depression, not TCA profile; TCAs do not primarily block
VMAT2.
, • Incorrect (C): α2-autoreceptor activation would reduce NE
release and lessen tremor; TCAs do not directly activate
α2-autoreceptors.
• Incorrect (D): TCAs are not GABA_A agonists; GABA_A
agonism would more likely produce sedation, not
sympathetic-like tremor and anticholinergic effects.
Teaching Point
Transporter blockade raises synaptic monoamines; TCAs’
anticholinergic effects cause autonomic side effects.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission — Calcium-dependent
release & SNARE
Stem
A 28-year-old patient with bipolar depression is markedly
responsive to lithium but develops worsening fatigue when
given a drug that interferes with presynaptic calcium influx.
Based on calcium-dependent exocytosis, which pharmacologic
action most directly diminishes neurotransmitter release and
could explain decreased mood/energy?
, Options
A. Blockade of presynaptic voltage-gated calcium channels
(VGCCs)
B. Inhibition of postsynaptic NMDA receptors
C. Enhancement of presynaptic vesicular docking proteins
(SNARE complex)
D. Activation of presynaptic nicotinic receptors increasing
release
Correct Answer
A
Rationales
• Correct (A): Neurotransmitter exocytosis requires
presynaptic VGCC-mediated Ca²⁺ influx; blocking VGCCs
reduces release broadly, producing decreased
monoaminergic transmission which can worsen
mood/energy. Stahl highlights the central role of Ca²⁺ entry
in vesicular release.
• Incorrect (B): NMDA receptor inhibition affects
postsynaptic excitatory signaling, not the primary
mechanism for presynaptic transmitter release.
• Incorrect (C): Enhancing SNARE function would increase,
not decrease, vesicular release.
• Incorrect (D): Presynaptic nicotinic receptor activation
typically increases release; that would enhance, not
diminish, neurotransmission.
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 45-year-old patient with major depressive disorder reports
sudden episodes of increased anxiety and tremor shortly after
starting a high-dose tricyclic antidepressant (TCA). He also
reports dry mouth and constipation. Considering presynaptic
vesicular handling and anticholinergic/adrenergic effects, which
mechanism best explains the new tremor and autonomic
symptoms?
,Options
A. TCA blockade of vesicular monoamine transporter (VMAT2)
causing cytosolic monoamine depletion
B. TCA inhibition of monoamine reuptake transporters
increasing synaptic monoamines and anticholinergic
antagonism at muscarinic receptors
C. TCA activation of presynaptic α2-autoreceptors reducing
norepinephrine release
D. TCA agonism at postsynaptic GABA_A receptors causing
paradoxical excitation
Correct Answer
B
Rationales
• Correct (B): TCAs inhibit SERT and NET, increasing synaptic
monoamine levels which can provoke anxiety and tremor
through enhanced noradrenergic tone; TCAs also have
strong muscarinic antagonism explaining dry mouth and
constipation. Stahl emphasizes how transporter blockade
increases synaptic neurotransmitter availability producing
both therapeutic and noradrenergic/adrenergic side
effects.
• Incorrect (A): VMAT2 blockade reduces vesicular storage
(seen with tetrabenazine), causing parkinsonism and
depression, not TCA profile; TCAs do not primarily block
VMAT2.
, • Incorrect (C): α2-autoreceptor activation would reduce NE
release and lessen tremor; TCAs do not directly activate
α2-autoreceptors.
• Incorrect (D): TCAs are not GABA_A agonists; GABA_A
agonism would more likely produce sedation, not
sympathetic-like tremor and anticholinergic effects.
Teaching Point
Transporter blockade raises synaptic monoamines; TCAs’
anticholinergic effects cause autonomic side effects.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission — Calcium-dependent
release & SNARE
Stem
A 28-year-old patient with bipolar depression is markedly
responsive to lithium but develops worsening fatigue when
given a drug that interferes with presynaptic calcium influx.
Based on calcium-dependent exocytosis, which pharmacologic
action most directly diminishes neurotransmitter release and
could explain decreased mood/energy?
, Options
A. Blockade of presynaptic voltage-gated calcium channels
(VGCCs)
B. Inhibition of postsynaptic NMDA receptors
C. Enhancement of presynaptic vesicular docking proteins
(SNARE complex)
D. Activation of presynaptic nicotinic receptors increasing
release
Correct Answer
A
Rationales
• Correct (A): Neurotransmitter exocytosis requires
presynaptic VGCC-mediated Ca²⁺ influx; blocking VGCCs
reduces release broadly, producing decreased
monoaminergic transmission which can worsen
mood/energy. Stahl highlights the central role of Ca²⁺ entry
in vesicular release.
• Incorrect (B): NMDA receptor inhibition affects
postsynaptic excitatory signaling, not the primary
mechanism for presynaptic transmitter release.
• Incorrect (C): Enhancing SNARE function would increase,
not decrease, vesicular release.
• Incorrect (D): Presynaptic nicotinic receptor activation
typically increases release; that would enhance, not
diminish, neurotransmission.
