STAHL'S ESSENTIAL PSYCHOPHARMACOLOGY
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission — Synaptic vesicular
release & calcium-dependence
Stem
A 32-year-old patient with major depressive disorder reports
sudden worsening of concentration and new cognitive
“slowing” after starting a medication that reduces synaptic
vesicular release. He has no cardiac disease. Which mechanism
most likely explains his acute cognitive slowing?
,A. Inhibition of vesicular monoamine transporter (VMAT2)
reducing synaptic monoamine availability
B. Blockade of postsynaptic NMDA receptors diminishing
glutamatergic transmission
C. Increased presynaptic reuptake of monoamines via
transporters (e.g., SERT/NET)
D. Activation of presynaptic autoreceptors decreasing
neurotransmitter release
Correct answer
A
Rationales
Correct: Inhibition of VMAT2 reduces vesicular loading of
monoamines (serotonin, norepinephrine, dopamine), causing
broad reductions in synaptic monoamine release; Stahl links
reduced monoaminergic tone to cognitive slowing and
psychomotor retardation. VMAT2 inhibition therefore explains
the diffuse cognitive effects.
Incorrect A→B: NMDA antagonism can cause dissociation and
cognitive effects but the stem specifies a drug that reduces
vesicular release; NMDA blockade is a postsynaptic ionotropic
mechanism mismatch.
Incorrect A→C: Increased reuptake would lower synaptic
monoamines but via transporter action rather than impairing
vesicular storage — clinical onset and pattern differ from
VMAT2 effects.
Incorrect A→D: Autoreceptor activation decreases release but
,typically produces a more selective, reversible decrease and is
mechanistically distinct from vesicular depletion.
Teaching point
VMAT2 blockade causes global monoamine depletion →
cognitive slowing and psychomotor slowing.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission — Neurotransmitter
synthesis & rate-limiting enzymes
Stem
A 45-year-old woman with bipolar depression is pregnant (first
trimester). You need to explain how inhibition of a
neurotransmitter’s rate-limiting enzyme could rapidly deplete
that transmitter and affect fetal development. Which enzymatic
inhibition best fits an agent that directly prevents synthesis of
norepinephrine and dopamine?
A. Inhibition of tyrosine hydroxylase
B. Inhibition of tryptophan hydroxylase
C. Inhibition of glutamic acid decarboxylase (GAD)
D. Inhibition of choline acetyltransferase (ChAT)
, Correct answer
A
Rationales
Correct: Tyrosine hydroxylase is the rate-limiting enzyme for
catecholamine synthesis (dopamine → norepinephrine).
Inhibiting it would directly reduce catecholamine production;
Stahl emphasizes rate-limiting enzymes’ central role in
transmitter availability. This is the mechanism that would most
directly deplete NE and DA.
Incorrect B: Tryptophan hydroxylase is the rate-limiting enzyme
for serotonin synthesis, not catecholamines.
Incorrect C: GAD synthesizes GABA from glutamate — unrelated
to NE/DA synthesis.
Incorrect D: ChAT synthesizes acetylcholine — not involved in
catecholamine synthesis.
Teaching point
Rate-limiting enzymes (e.g., tyrosine hydroxylase) critically
determine transmitter availability.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
3
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission — Synaptic vesicular
release & calcium-dependence
Stem
A 32-year-old patient with major depressive disorder reports
sudden worsening of concentration and new cognitive
“slowing” after starting a medication that reduces synaptic
vesicular release. He has no cardiac disease. Which mechanism
most likely explains his acute cognitive slowing?
,A. Inhibition of vesicular monoamine transporter (VMAT2)
reducing synaptic monoamine availability
B. Blockade of postsynaptic NMDA receptors diminishing
glutamatergic transmission
C. Increased presynaptic reuptake of monoamines via
transporters (e.g., SERT/NET)
D. Activation of presynaptic autoreceptors decreasing
neurotransmitter release
Correct answer
A
Rationales
Correct: Inhibition of VMAT2 reduces vesicular loading of
monoamines (serotonin, norepinephrine, dopamine), causing
broad reductions in synaptic monoamine release; Stahl links
reduced monoaminergic tone to cognitive slowing and
psychomotor retardation. VMAT2 inhibition therefore explains
the diffuse cognitive effects.
Incorrect A→B: NMDA antagonism can cause dissociation and
cognitive effects but the stem specifies a drug that reduces
vesicular release; NMDA blockade is a postsynaptic ionotropic
mechanism mismatch.
Incorrect A→C: Increased reuptake would lower synaptic
monoamines but via transporter action rather than impairing
vesicular storage — clinical onset and pattern differ from
VMAT2 effects.
Incorrect A→D: Autoreceptor activation decreases release but
,typically produces a more selective, reversible decrease and is
mechanistically distinct from vesicular depletion.
Teaching point
VMAT2 blockade causes global monoamine depletion →
cognitive slowing and psychomotor slowing.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission — Neurotransmitter
synthesis & rate-limiting enzymes
Stem
A 45-year-old woman with bipolar depression is pregnant (first
trimester). You need to explain how inhibition of a
neurotransmitter’s rate-limiting enzyme could rapidly deplete
that transmitter and affect fetal development. Which enzymatic
inhibition best fits an agent that directly prevents synthesis of
norepinephrine and dopamine?
A. Inhibition of tyrosine hydroxylase
B. Inhibition of tryptophan hydroxylase
C. Inhibition of glutamic acid decarboxylase (GAD)
D. Inhibition of choline acetyltransferase (ChAT)
, Correct answer
A
Rationales
Correct: Tyrosine hydroxylase is the rate-limiting enzyme for
catecholamine synthesis (dopamine → norepinephrine).
Inhibiting it would directly reduce catecholamine production;
Stahl emphasizes rate-limiting enzymes’ central role in
transmitter availability. This is the mechanism that would most
directly deplete NE and DA.
Incorrect B: Tryptophan hydroxylase is the rate-limiting enzyme
for serotonin synthesis, not catecholamines.
Incorrect C: GAD synthesizes GABA from glutamate — unrelated
to NE/DA synthesis.
Incorrect D: ChAT synthesizes acetylcholine — not involved in
catecholamine synthesis.
Teaching point
Rate-limiting enzymes (e.g., tyrosine hydroxylase) critically
determine transmitter availability.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
3
