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 Release &
Vesicular Storage
Stem
A 42-year-old woman with major depressive disorder has
limited benefit from an SSRI trial. Her psychiatrist considers
augmenting with a medication that reduces presynaptic
monoamine vesicular storage to increase cytosolic monoamine
metabolism and reduce tonic neurotransmitter release. Which
pharmacologic target best matches this mechanism?
Options
A. Inhibition of vesicular monoamine transporter (VMAT2)
,B. Blockade of monoamine oxidase (MAO)
C. Inhibition of plasma membrane monoamine transporters
(e.g., SERT, NET)
D. Antagonism of presynaptic autoreceptors (e.g., 5-HT1A
autoreceptor blockade)
Correct Answer
A
Rationales
Correct (A): VMAT2 inhibition prevents uptake of monoamines
into vesicles, increasing cytosolic monoamines and enhancing
their breakdown by MAO, thereby reducing regulated vesicular
release. Stahl describes VMAT function and how VMAT blockade
alters storage and synaptic availability.
Incorrect (B): MAO blockade decreases monoamine
metabolism, increasing monoamine levels; this does not reduce
vesicular storage nor increase cytosolic breakdown as
described.
Incorrect (C): Inhibiting SERT/NET increases extracellular
reuptake blockade and synaptic monoamine levels, opposite to
reducing vesicular storage.
Incorrect (D): Antagonizing presynaptic autoreceptors increases
release probability but does not directly inhibit vesicular
storage.
Teaching Point
VMAT2 inhibition reduces vesicular monoamine storage, raising
cytosolic degradation and altering synaptic release.
,Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission — Quantal Release &
Synaptic Dynamics
Stem
A patient’s manic symptoms appear linked to excessive phasic
dopaminergic signaling. You must choose an intervention that
specifically reduces quantal (vesicle-mediated)
neurotransmitter release probability without blocking
postsynaptic receptors. Which mechanism best accomplishes
that?
Options
A. Enhancing presynaptic GABA_B heteroreceptor activation
that decreases calcium influx
B. Direct blockade of postsynaptic D2 receptors
C. Blocking the vesicular release machinery (SNARE complex)
postsynaptically
D. Inhibition of postsynaptic ionotropic glutamate receptors
Correct Answer
A
, Rationales
Correct (A): Activation of presynaptic G_i/o-coupled GABA_B
heteroreceptors reduces presynaptic calcium entry, lowering
vesicular release probability—Stahl explains heteroreceptor
modulation of release.
Incorrect (B): Blocking postsynaptic D2 receptors reduces
postsynaptic response but does not reduce presynaptic quantal
release probability.
Incorrect (C): SNARE complex blockade would reduce vesicular
release but is presynaptic; option states postsynaptic blockade,
which is incorrect and implausible clinically.
Incorrect (D): Inhibiting postsynaptic glutamate receptors
reduces excitatory postsynaptic potentials but not presynaptic
quantal release probability.
Teaching Point
Presynaptic G_i/o receptors modulate calcium-dependent
quantal release, altering neurotransmission without
postsynaptic blockade.
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 Release &
Vesicular Storage
Stem
A 42-year-old woman with major depressive disorder has
limited benefit from an SSRI trial. Her psychiatrist considers
augmenting with a medication that reduces presynaptic
monoamine vesicular storage to increase cytosolic monoamine
metabolism and reduce tonic neurotransmitter release. Which
pharmacologic target best matches this mechanism?
Options
A. Inhibition of vesicular monoamine transporter (VMAT2)
,B. Blockade of monoamine oxidase (MAO)
C. Inhibition of plasma membrane monoamine transporters
(e.g., SERT, NET)
D. Antagonism of presynaptic autoreceptors (e.g., 5-HT1A
autoreceptor blockade)
Correct Answer
A
Rationales
Correct (A): VMAT2 inhibition prevents uptake of monoamines
into vesicles, increasing cytosolic monoamines and enhancing
their breakdown by MAO, thereby reducing regulated vesicular
release. Stahl describes VMAT function and how VMAT blockade
alters storage and synaptic availability.
Incorrect (B): MAO blockade decreases monoamine
metabolism, increasing monoamine levels; this does not reduce
vesicular storage nor increase cytosolic breakdown as
described.
Incorrect (C): Inhibiting SERT/NET increases extracellular
reuptake blockade and synaptic monoamine levels, opposite to
reducing vesicular storage.
Incorrect (D): Antagonizing presynaptic autoreceptors increases
release probability but does not directly inhibit vesicular
storage.
Teaching Point
VMAT2 inhibition reduces vesicular monoamine storage, raising
cytosolic degradation and altering synaptic release.
,Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission — Quantal Release &
Synaptic Dynamics
Stem
A patient’s manic symptoms appear linked to excessive phasic
dopaminergic signaling. You must choose an intervention that
specifically reduces quantal (vesicle-mediated)
neurotransmitter release probability without blocking
postsynaptic receptors. Which mechanism best accomplishes
that?
Options
A. Enhancing presynaptic GABA_B heteroreceptor activation
that decreases calcium influx
B. Direct blockade of postsynaptic D2 receptors
C. Blocking the vesicular release machinery (SNARE complex)
postsynaptically
D. Inhibition of postsynaptic ionotropic glutamate receptors
Correct Answer
A
, Rationales
Correct (A): Activation of presynaptic G_i/o-coupled GABA_B
heteroreceptors reduces presynaptic calcium entry, lowering
vesicular release probability—Stahl explains heteroreceptor
modulation of release.
Incorrect (B): Blocking postsynaptic D2 receptors reduces
postsynaptic response but does not reduce presynaptic quantal
release probability.
Incorrect (C): SNARE complex blockade would reduce vesicular
release but is presynaptic; option states postsynaptic blockade,
which is incorrect and implausible clinically.
Incorrect (D): Inhibiting postsynaptic glutamate receptors
reduces excitatory postsynaptic potentials but not presynaptic
quantal release probability.
Teaching Point
Presynaptic G_i/o receptors modulate calcium-dependent
quantal release, altering neurotransmission without
postsynaptic blockade.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
3
