Stahl's Essential Psychopharmacology
Neuroscientific Basis and Practical Applications
5th Edition
Author(s)Stephen M. Stahl
TEST BANK
Question 1
Reference: Ch. 1, Chemical Neurotransmission
Question Stem: A patient with Parkinson's disease is prescribed
levodopa. The therapeutic efficacy of this precursor molecule is
most directly dependent on which of the following presynaptic
processes?
A. Enzymatic degradation by monoamine oxidase (MAO)
B. Vesicular packaging via the vesicular monoamine transporter
(VMAT)
C. Reuptake from the synaptic cleft via the dopamine
transporter (DAT)
D. Signal termination via autoreceptor feedback
Correct Answer: B
Rationales:
, • Correct: Levodopa is converted to dopamine inside the
presynaptic neuron. For dopamine to be released in a
regulated manner, it must be packaged into synaptic
vesicles by the vesicular monoamine transporter (VMAT).
Without this packaging, cytosolic dopamine would be
degraded and not available for release.
• Incorrect A: Enzymatic degradation by MAO is a process
that inactivates dopamine, reducing its availability, not
enabling its therapeutic efficacy.
• Incorrect C: The dopamine transporter (DAT) is primarily
responsible for reuptake and termination of dopamine's
action, not for the initial packaging and release of
synthesized dopamine.
• Incorrect D: Autoreceptor feedback is a regulatory
mechanism that modulates release, but it is not the
fundamental process required for storing and releasing the
newly synthesized dopamine from its precursor.
Teaching Point: Precursor loading requires vesicular packaging
to become a functional, releasable neurotransmitter.
Citation: Ch. 1, Chemical Neurotransmission, Stahl's Essential
Psychopharmacology, 5th Edition
Question 2
Reference: Ch. 1, Chemical Neurotransmission
,Question Stem: A nursing student is explaining the mechanism
of action of benzodiazepines to a patient. The student correctly
states that benzodiazepines exert their effect by:
A. Directly activating the GABA-A receptor ion channel to allow
chloride influx.
B. Blocking the reuptake of GABA from the synaptic cleft,
prolonging its action.
C. Acting as positive allosteric modulators to enhance GABA's
effect when it binds.
D. Inhibiting the enzyme GABA transaminase, thereby
increasing GABA levels.
Correct Answer: C
Rationales:
• Correct: Benzodiazepines do not activate the GABA-A
receptor themselves. Instead, they bind to an allosteric site
on the receptor complex, which increases the frequency of
chloride channel opening when GABA is also bound,
thereby potentiating the inhibitory effect of GABA.
• Incorrect A: This describes the action of a direct agonist,
such as muscimol, not a benzodiazepine.
• Incorrect B: This is the mechanism for GABA reuptake
inhibitors, such as tiagabine, not benzodiazepines.
• Incorrect D: This is the mechanism of action for GABA
transaminase inhibitors, such as valproate or vigabatrin.
, Teaching Point: Benzodiazepines are positive allosteric
modulators, not direct agonists, at the GABA-A receptor.
Citation: Ch. 1, Chemical Neurotransmission, Stahl's Essential
Psychopharmacology, 5th Edition
Question 3
Reference: Ch. 1, Chemical Neurotransmission
Question Stem: When discussing the therapeutic lag of SSRIs
with a patient, the psychiatric-mental health nurse practitioner
explains that the delay in antidepressant effect is best
attributed to:
A. The time required to achieve a steady-state plasma
concentration of the drug.
B. Initial overstimulation of postsynaptic serotonin receptors
causing side effects.
C. Downregulation of serotonin transporters (SERT) in the
presynaptic membrane.
D. Desensitization of somatodendritic 5-HT1A autoreceptors,
leading to increased serotonin release.
Correct Answer: D
Rationales:
• Correct: The therapeutic lag is theorized to be due to the
time it takes for the sustained increase in synaptic
serotonin to desensitize the somatodendritic 5-HT1A
Neuroscientific Basis and Practical Applications
5th Edition
Author(s)Stephen M. Stahl
TEST BANK
Question 1
Reference: Ch. 1, Chemical Neurotransmission
Question Stem: A patient with Parkinson's disease is prescribed
levodopa. The therapeutic efficacy of this precursor molecule is
most directly dependent on which of the following presynaptic
processes?
A. Enzymatic degradation by monoamine oxidase (MAO)
B. Vesicular packaging via the vesicular monoamine transporter
(VMAT)
C. Reuptake from the synaptic cleft via the dopamine
transporter (DAT)
D. Signal termination via autoreceptor feedback
Correct Answer: B
Rationales:
, • Correct: Levodopa is converted to dopamine inside the
presynaptic neuron. For dopamine to be released in a
regulated manner, it must be packaged into synaptic
vesicles by the vesicular monoamine transporter (VMAT).
Without this packaging, cytosolic dopamine would be
degraded and not available for release.
• Incorrect A: Enzymatic degradation by MAO is a process
that inactivates dopamine, reducing its availability, not
enabling its therapeutic efficacy.
• Incorrect C: The dopamine transporter (DAT) is primarily
responsible for reuptake and termination of dopamine's
action, not for the initial packaging and release of
synthesized dopamine.
• Incorrect D: Autoreceptor feedback is a regulatory
mechanism that modulates release, but it is not the
fundamental process required for storing and releasing the
newly synthesized dopamine from its precursor.
Teaching Point: Precursor loading requires vesicular packaging
to become a functional, releasable neurotransmitter.
Citation: Ch. 1, Chemical Neurotransmission, Stahl's Essential
Psychopharmacology, 5th Edition
Question 2
Reference: Ch. 1, Chemical Neurotransmission
,Question Stem: A nursing student is explaining the mechanism
of action of benzodiazepines to a patient. The student correctly
states that benzodiazepines exert their effect by:
A. Directly activating the GABA-A receptor ion channel to allow
chloride influx.
B. Blocking the reuptake of GABA from the synaptic cleft,
prolonging its action.
C. Acting as positive allosteric modulators to enhance GABA's
effect when it binds.
D. Inhibiting the enzyme GABA transaminase, thereby
increasing GABA levels.
Correct Answer: C
Rationales:
• Correct: Benzodiazepines do not activate the GABA-A
receptor themselves. Instead, they bind to an allosteric site
on the receptor complex, which increases the frequency of
chloride channel opening when GABA is also bound,
thereby potentiating the inhibitory effect of GABA.
• Incorrect A: This describes the action of a direct agonist,
such as muscimol, not a benzodiazepine.
• Incorrect B: This is the mechanism for GABA reuptake
inhibitors, such as tiagabine, not benzodiazepines.
• Incorrect D: This is the mechanism of action for GABA
transaminase inhibitors, such as valproate or vigabatrin.
, Teaching Point: Benzodiazepines are positive allosteric
modulators, not direct agonists, at the GABA-A receptor.
Citation: Ch. 1, Chemical Neurotransmission, Stahl's Essential
Psychopharmacology, 5th Edition
Question 3
Reference: Ch. 1, Chemical Neurotransmission
Question Stem: When discussing the therapeutic lag of SSRIs
with a patient, the psychiatric-mental health nurse practitioner
explains that the delay in antidepressant effect is best
attributed to:
A. The time required to achieve a steady-state plasma
concentration of the drug.
B. Initial overstimulation of postsynaptic serotonin receptors
causing side effects.
C. Downregulation of serotonin transporters (SERT) in the
presynaptic membrane.
D. Desensitization of somatodendritic 5-HT1A autoreceptors,
leading to increased serotonin release.
Correct Answer: D
Rationales:
• Correct: The therapeutic lag is theorized to be due to the
time it takes for the sustained increase in synaptic
serotonin to desensitize the somatodendritic 5-HT1A
