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 and
calcium dependence
Stem
A 32-year-old patient reports new onset tremor and
restlessness after starting a novel antidepressant. The
prescriber suspects the agent increased synaptic monoamine
availability by enhancing presynaptic release. Which
presynaptic process, if enhanced, most directly increases
quantal neurotransmitter release during an action potential?
A. Increased vesicular monoamine transporter (VMAT) activity,
increasing vesicular transmitter concentration
,B. Increased presynaptic calcium influx at voltage-gated calcium
channels during depolarization
C. Upregulation of presynaptic autoreceptors reducing
transmitter synthesis
D. Increased activity of reuptake transporters removing
transmitter from the cleft
Correct answer
B
Rationale — Correct (B)
Quantal release of neurotransmitter during an action potential
is directly triggered by calcium influx through presynaptic
voltage-gated Ca²⁺ channels; greater Ca²⁺ entry increases vesicle
fusion and release probability. Stahl emphasizes that Ca²⁺
coupling to the release machinery is the key trigger for
exocytosis, so enhancing Ca²⁺ entry raises synaptic release and
extracellular transmitter. This mechanism best explains an acute
increase in synaptic monoamine availability causing activation
side effects.
Rationales — Incorrect
A. Increasing VMAT raises vesicular content but does not
directly change the immediate probability of Ca²⁺-triggered
vesicle fusion.
C. Upregulation of autoreceptors would decrease, not increase,
release and synthesis.
D. Increased transporter activity removes transmitter from the
,cleft, lowering extracellular levels rather than increasing
release.
Teaching point
Presynaptic Ca²⁺ influx directly controls vesicular
neurotransmitter release probability.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission — Receptors: ionotropic
vs metabotropic
Stem
A 46-year-old patient with anxiety experiences rapid relief from
an intravenous agent that acts on postsynaptic GABAA_AA
receptors, but the clinician wants a daily oral agent that
produces longer-lasting modulation via intracellular signaling.
According to the ionotropic/metabotropic distinction, which
property differentiates an oral agent acting at metabotropic
receptors from the IV GABAA_AA agonist?
A. Metabotropic receptors produce faster millisecond ion flux
than ionotropic receptors.
B. Metabotropic receptors signal via G proteins and second
messengers, producing slower, longer-lasting effects.
, C. Ionotropic receptors do not change postsynaptic membrane
conductance.
D. Metabotropic receptors are only presynaptic and thus cannot
modulate postsynaptic excitability.
Correct answer
B
Rationale — Correct (B)
Metabotropic receptors (GPCRs) couple to G proteins and
second-messenger cascades, mediating modulatory effects that
are slower to onset but longer in duration than the direct ion-
channel gating of ionotropic receptors like GABAA_AA. Stahl’s
framework highlights that metabotropic signaling alters
downstream cellular states (e.g., phosphorylation, gene
expression) and is suited for sustained therapeutic modulation.
Rationales — Incorrect
A. Ionotropic receptors produce the fastest millisecond-scale
ion flux; metabotropic are slower.
C. Ionotropic receptors directly change membrane conductance
through ion channels.
D. Metabotropic receptors exist both pre- and postsynaptically
and modulate excitability at either site.
Teaching point
GPCR (metabotropic) signaling: slower onset, second-
messenger cascades, longer modulation than ionotropic
channels.
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission — Synaptic release and
calcium dependence
Stem
A 32-year-old patient reports new onset tremor and
restlessness after starting a novel antidepressant. The
prescriber suspects the agent increased synaptic monoamine
availability by enhancing presynaptic release. Which
presynaptic process, if enhanced, most directly increases
quantal neurotransmitter release during an action potential?
A. Increased vesicular monoamine transporter (VMAT) activity,
increasing vesicular transmitter concentration
,B. Increased presynaptic calcium influx at voltage-gated calcium
channels during depolarization
C. Upregulation of presynaptic autoreceptors reducing
transmitter synthesis
D. Increased activity of reuptake transporters removing
transmitter from the cleft
Correct answer
B
Rationale — Correct (B)
Quantal release of neurotransmitter during an action potential
is directly triggered by calcium influx through presynaptic
voltage-gated Ca²⁺ channels; greater Ca²⁺ entry increases vesicle
fusion and release probability. Stahl emphasizes that Ca²⁺
coupling to the release machinery is the key trigger for
exocytosis, so enhancing Ca²⁺ entry raises synaptic release and
extracellular transmitter. This mechanism best explains an acute
increase in synaptic monoamine availability causing activation
side effects.
Rationales — Incorrect
A. Increasing VMAT raises vesicular content but does not
directly change the immediate probability of Ca²⁺-triggered
vesicle fusion.
C. Upregulation of autoreceptors would decrease, not increase,
release and synthesis.
D. Increased transporter activity removes transmitter from the
,cleft, lowering extracellular levels rather than increasing
release.
Teaching point
Presynaptic Ca²⁺ influx directly controls vesicular
neurotransmitter release probability.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission — Receptors: ionotropic
vs metabotropic
Stem
A 46-year-old patient with anxiety experiences rapid relief from
an intravenous agent that acts on postsynaptic GABAA_AA
receptors, but the clinician wants a daily oral agent that
produces longer-lasting modulation via intracellular signaling.
According to the ionotropic/metabotropic distinction, which
property differentiates an oral agent acting at metabotropic
receptors from the IV GABAA_AA agonist?
A. Metabotropic receptors produce faster millisecond ion flux
than ionotropic receptors.
B. Metabotropic receptors signal via G proteins and second
messengers, producing slower, longer-lasting effects.
, C. Ionotropic receptors do not change postsynaptic membrane
conductance.
D. Metabotropic receptors are only presynaptic and thus cannot
modulate postsynaptic excitability.
Correct answer
B
Rationale — Correct (B)
Metabotropic receptors (GPCRs) couple to G proteins and
second-messenger cascades, mediating modulatory effects that
are slower to onset but longer in duration than the direct ion-
channel gating of ionotropic receptors like GABAA_AA. Stahl’s
framework highlights that metabotropic signaling alters
downstream cellular states (e.g., phosphorylation, gene
expression) and is suited for sustained therapeutic modulation.
Rationales — Incorrect
A. Ionotropic receptors produce the fastest millisecond-scale
ion flux; metabotropic are slower.
C. Ionotropic receptors directly change membrane conductance
through ion channels.
D. Metabotropic receptors exist both pre- and postsynaptically
and modulate excitability at either site.
Teaching point
GPCR (metabotropic) signaling: slower onset, second-
messenger cascades, longer modulation than ionotropic
channels.
