STAHL'S ESSENTIAL PSYCHOPHARMACOLOGY
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission
PMHNP-Level Question Stem
A 34-year-old patient with major depressive symptoms shows
early partial improvement on a selective serotonin reuptake
inhibitor (SSRI) after 3 weeks but complains of persistent
insomnia and emotional blunting. You consider strategies that
act on presynaptic autoreceptors or the serotonin transporter
to accelerate or augment response. Which mechanism-based
strategy best fits Stahl’s description of accelerating serotonergic
synaptic availability without directly stimulating postsynaptic 5-
HT receptors?
,Options
A. Add a 5-HT1A partial agonist to desensitize somatodendritic
autoreceptors and increase serotonergic firing.
B. Add a 5-HT2A antagonist to reduce downstream postsynaptic
excitability.
C. Switch to a monoamine oxidase inhibitor to prevent
enzymatic serotonin breakdown.
D. Add a postsynaptic 5-HT1A full agonist to directly stimulate
cortical serotonin receptors.
Correct Answer
A
Rationales
Correct (A): Stahl describes how somatodendritic 5-HT1A
autoreceptors inhibit serotonergic neuron firing; a 5-HT1A
partial agonist can accelerate clinical response by desensitizing
autoreceptors and increasing serotonin release while preserving
transporter blockade effects. This increases presynaptic firing
and synaptic 5-HT availability without direct strong postsynaptic
overstimulation.
Incorrect (B): A 5-HT2A antagonist affects postsynaptic signaling
and may ameliorate some side effects but does not accelerate
serotonergic neuron firing via autoreceptor modulation.
Incorrect (C): MAO inhibition increases extracellular serotonin
broadly but is a non-selective enzymatic approach with dietary
and safety concerns and is not a targeted autoreceptor strategy
described for accelerating SSRI onset.
,Incorrect (D): A postsynaptic 5-HT1A full agonist stimulates
postsynaptic receptors but does not desensitize presynaptic
somatodendritic autoreceptors to increase neuron firing as
Stahl outlines.
Teaching Point
Desensitizing 5-HT1A autoreceptors increases serotonergic
firing and speeds SSRI effects.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission
PMHNP-Level Question Stem
A 67-year-old patient with generalized anxiety disorder is
particularly vulnerable to anticholinergic adverse effects
(confusion, constipation, urinary retention). You must choose
an anxiolytic strategy that reduces synaptic hyperexcitability
while minimizing cholinergic blockade. Which mechanism best
satisfies Stahl’s neurochemical principles?
Options
A. Use a GABA_A positive allosteric modulator to enhance
inhibitory chloride conductance.
B. Use a non-selective anticholinergic antihistamine to reduce
, arousal.
C. Use a high-affinity muscarinic antagonist to dampen limbic
cholinergic tone.
D. Use a serotonin releaser to indirectly inhibit cholinergic
interneurons.
Correct Answer
A
Rationales
Correct (A): Stahl emphasizes GABA as the principal inhibitory
neurotransmitter; positive allosteric modulation of GABA_A
increases chloride influx and network inhibition, providing
anxiolysis without anticholinergic risk. This matches
mechanism-driven selection for an older adult.
Incorrect (B): Non-selective H1 antihistamines often have
anticholinergic properties and sedation; they raise risks of
confusion in older adults, contrary to the stated goal.
Incorrect (C): Muscarinic antagonism directly causes the
anticholinergic adverse effects you wish to avoid; therefore, it is
inappropriate.
Incorrect (D): Serotonin releasers are not a targeted approach
for acute inhibitory enhancement and may have unpredictable
downstream effects; Stahl does not recommend this for
cholinergic-sensitive elderly patients.
Teaching Point
Enhancing GABA_A inhibition provides anxiolysis without
anticholinergic burden in older adults.
NEUROSCIENTIFIC BASIS AND PRACTICAL
APPLICATIONS
5TH EDITION
AUTHOR(S)STEPHEN M. STAHL
TEST BANK
1
Reference
Ch. 1 — Chemical Neurotransmission
PMHNP-Level Question Stem
A 34-year-old patient with major depressive symptoms shows
early partial improvement on a selective serotonin reuptake
inhibitor (SSRI) after 3 weeks but complains of persistent
insomnia and emotional blunting. You consider strategies that
act on presynaptic autoreceptors or the serotonin transporter
to accelerate or augment response. Which mechanism-based
strategy best fits Stahl’s description of accelerating serotonergic
synaptic availability without directly stimulating postsynaptic 5-
HT receptors?
,Options
A. Add a 5-HT1A partial agonist to desensitize somatodendritic
autoreceptors and increase serotonergic firing.
B. Add a 5-HT2A antagonist to reduce downstream postsynaptic
excitability.
C. Switch to a monoamine oxidase inhibitor to prevent
enzymatic serotonin breakdown.
D. Add a postsynaptic 5-HT1A full agonist to directly stimulate
cortical serotonin receptors.
Correct Answer
A
Rationales
Correct (A): Stahl describes how somatodendritic 5-HT1A
autoreceptors inhibit serotonergic neuron firing; a 5-HT1A
partial agonist can accelerate clinical response by desensitizing
autoreceptors and increasing serotonin release while preserving
transporter blockade effects. This increases presynaptic firing
and synaptic 5-HT availability without direct strong postsynaptic
overstimulation.
Incorrect (B): A 5-HT2A antagonist affects postsynaptic signaling
and may ameliorate some side effects but does not accelerate
serotonergic neuron firing via autoreceptor modulation.
Incorrect (C): MAO inhibition increases extracellular serotonin
broadly but is a non-selective enzymatic approach with dietary
and safety concerns and is not a targeted autoreceptor strategy
described for accelerating SSRI onset.
,Incorrect (D): A postsynaptic 5-HT1A full agonist stimulates
postsynaptic receptors but does not desensitize presynaptic
somatodendritic autoreceptors to increase neuron firing as
Stahl outlines.
Teaching Point
Desensitizing 5-HT1A autoreceptors increases serotonergic
firing and speeds SSRI effects.
Citation
Stahl, S. M. (2021). Essential Psychopharmacology (5th ed.). Ch.
1.
2
Reference
Ch. 1 — Chemical Neurotransmission
PMHNP-Level Question Stem
A 67-year-old patient with generalized anxiety disorder is
particularly vulnerable to anticholinergic adverse effects
(confusion, constipation, urinary retention). You must choose
an anxiolytic strategy that reduces synaptic hyperexcitability
while minimizing cholinergic blockade. Which mechanism best
satisfies Stahl’s neurochemical principles?
Options
A. Use a GABA_A positive allosteric modulator to enhance
inhibitory chloride conductance.
B. Use a non-selective anticholinergic antihistamine to reduce
, arousal.
C. Use a high-affinity muscarinic antagonist to dampen limbic
cholinergic tone.
D. Use a serotonin releaser to indirectly inhibit cholinergic
interneurons.
Correct Answer
A
Rationales
Correct (A): Stahl emphasizes GABA as the principal inhibitory
neurotransmitter; positive allosteric modulation of GABA_A
increases chloride influx and network inhibition, providing
anxiolysis without anticholinergic risk. This matches
mechanism-driven selection for an older adult.
Incorrect (B): Non-selective H1 antihistamines often have
anticholinergic properties and sedation; they raise risks of
confusion in older adults, contrary to the stated goal.
Incorrect (C): Muscarinic antagonism directly causes the
anticholinergic adverse effects you wish to avoid; therefore, it is
inappropriate.
Incorrect (D): Serotonin releasers are not a targeted approach
for acute inhibitory enhancement and may have unpredictable
downstream effects; Stahl does not recommend this for
cholinergic-sensitive elderly patients.
Teaching Point
Enhancing GABA_A inhibition provides anxiolysis without
anticholinergic burden in older adults.
