STAHL'S ESSENTIAL PSYCHOPHARMACOLOGY
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission
Stem
A 34-year-old patient with major depressive disorder reports
increased anxiety and jitteriness during the first 2 weeks after
starting an SSRI. They have no cardiac disease. Which
mechanism most plausibly explains early SSRI-related activation
and guides short-term management?
Options
A. Acute postsynaptic 5-HT1A receptor upregulation causing
excessive serotonergic tone.
B. Presynaptic 5-HT1A autoreceptor activation causing reduced
,serotonergic neuron firing and transient downstream
imbalance.
C. Rapid blockade of the serotonin transporter (SERT) leading
immediately to maximal postsynaptic 5-HT2A stimulation.
D. Increased VMAT2 activity causing enhanced vesicular
serotonin release.
Correct answer
B
Rationales
Correct: Early SSRI effects are strongly influenced by presynaptic
5-HT1A autoreceptors; acute SERT blockade increases synaptic
5-HT, which activates autoreceptors and reduces firing —
producing a transient dysregulated serotonergic output that can
manifest as activation and anxiety until autoreceptor
desensitization occurs. Stahl emphasizes autoreceptor-
mediated negative feedback early in treatment.
A (incorrect): 5-HT1A postsynaptic upregulation is a longer-term
adaptation; acute upregulation would not cause early
activation.
C (incorrect): SERT blockade is immediate, but postsynaptic 5-
HT2A overstimulation alone does not explain the
autoregulatory decrease in serotonergic neuron firing that
causes early symptom fluctuation.
D (incorrect): VMAT2 modulation is not the acute mechanism of
SSRI activation.
,Teaching point
Presynaptic 5-HT1A autoreceptor activation causes transient
SSRI-related activation; desensitization mediates clinical
improvement.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission
Stem
A 28-year-old with ADHD and nicotine dependence requests a
medication that reduces nicotine cravings and has low seizure
risk. Considering neurotransmitter handling, which agent
selection most directly leverages transporter inhibition without
monoamine oxidase inhibition?
Options
A. Bupropion — dopamine and norepinephrine reuptake
inhibition (DAT/NET) with nicotinic receptor antagonism.
B. Selegiline patch — selective MAO-B inhibition increasing
synaptic dopamine.
C. Desipramine — strong NET inhibition with anticholinergic
effects.
D. Varenicline — full agonist at α4β2 nicotinic receptors.
, Correct answer
A
Rationales
Correct: Bupropion inhibits DAT and NET (reducing reuptake),
and its nicotinic receptor antagonism aids smoking cessation; its
mechanism is transporter inhibition rather than MAO inhibition
and it avoids MAOI dietary/interaction risks. Stahl describes
transporter blockade as a key mechanism for increasing
synaptic monoamines.
B (incorrect): MAO-B inhibition increases dopamine via reduced
catabolism but carries different interaction profile and is not
first-line for nicotine dependence in this context.
C (incorrect): Desipramine’s NET blockade is plausible for ADHD
but has anticholinergic/cardiac side effects and higher toxicity
risk than bupropion.
D (incorrect): Varenicline is a partial agonist at α4β2 (not full
agonist) and acts at nicotinic receptors, not via monoamine
transporters.
Teaching point
Targeting DAT/NET via reuptake inhibition increases synaptic
monoamines without MAO inhibition risks.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission
Stem
A 34-year-old patient with major depressive disorder reports
increased anxiety and jitteriness during the first 2 weeks after
starting an SSRI. They have no cardiac disease. Which
mechanism most plausibly explains early SSRI-related activation
and guides short-term management?
Options
A. Acute postsynaptic 5-HT1A receptor upregulation causing
excessive serotonergic tone.
B. Presynaptic 5-HT1A autoreceptor activation causing reduced
,serotonergic neuron firing and transient downstream
imbalance.
C. Rapid blockade of the serotonin transporter (SERT) leading
immediately to maximal postsynaptic 5-HT2A stimulation.
D. Increased VMAT2 activity causing enhanced vesicular
serotonin release.
Correct answer
B
Rationales
Correct: Early SSRI effects are strongly influenced by presynaptic
5-HT1A autoreceptors; acute SERT blockade increases synaptic
5-HT, which activates autoreceptors and reduces firing —
producing a transient dysregulated serotonergic output that can
manifest as activation and anxiety until autoreceptor
desensitization occurs. Stahl emphasizes autoreceptor-
mediated negative feedback early in treatment.
A (incorrect): 5-HT1A postsynaptic upregulation is a longer-term
adaptation; acute upregulation would not cause early
activation.
C (incorrect): SERT blockade is immediate, but postsynaptic 5-
HT2A overstimulation alone does not explain the
autoregulatory decrease in serotonergic neuron firing that
causes early symptom fluctuation.
D (incorrect): VMAT2 modulation is not the acute mechanism of
SSRI activation.
,Teaching point
Presynaptic 5-HT1A autoreceptor activation causes transient
SSRI-related activation; desensitization mediates clinical
improvement.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission
Stem
A 28-year-old with ADHD and nicotine dependence requests a
medication that reduces nicotine cravings and has low seizure
risk. Considering neurotransmitter handling, which agent
selection most directly leverages transporter inhibition without
monoamine oxidase inhibition?
Options
A. Bupropion — dopamine and norepinephrine reuptake
inhibition (DAT/NET) with nicotinic receptor antagonism.
B. Selegiline patch — selective MAO-B inhibition increasing
synaptic dopamine.
C. Desipramine — strong NET inhibition with anticholinergic
effects.
D. Varenicline — full agonist at α4β2 nicotinic receptors.
, Correct answer
A
Rationales
Correct: Bupropion inhibits DAT and NET (reducing reuptake),
and its nicotinic receptor antagonism aids smoking cessation; its
mechanism is transporter inhibition rather than MAO inhibition
and it avoids MAOI dietary/interaction risks. Stahl describes
transporter blockade as a key mechanism for increasing
synaptic monoamines.
B (incorrect): MAO-B inhibition increases dopamine via reduced
catabolism but carries different interaction profile and is not
first-line for nicotine dependence in this context.
C (incorrect): Desipramine’s NET blockade is plausible for ADHD
but has anticholinergic/cardiac side effects and higher toxicity
risk than bupropion.
D (incorrect): Varenicline is a partial agonist at α4β2 (not full
agonist) and acts at nicotinic receptors, not via monoamine
transporters.
Teaching point
Targeting DAT/NET via reuptake inhibition increases synaptic
monoamines without MAO inhibition risks.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
