Stahl's Essential Psychopharmacology
Neuroscientific Basis and Practical Applications
5th Edition
Author(s)Stephen M. Stahl
TEST BANK
Item 1
Reference: Ch. 1, Function: Presynaptic Events
Question Stem: A patient’s synaptic terminals fail to release
neurotransmitter despite normal action-potential arrival. Which
presynaptic mechanism is the most likely direct cause?
A. Failure of voltage-gated Ca²⁺ channel opening leading to
reduced intracellular Ca²⁺.
B. Increased postsynaptic receptor internalization decreasing
signal detection.
C. Excessive monoamine oxidase activity in the synaptic cleft
degrading neurotransmitter.
D. Upregulation of postsynaptic second-messenger systems
causing negative feedback.
Correct Answer: A
Rationales:
, • A (Correct): Neurotransmitter exocytosis is tightly coupled
to Ca²⁺ influx through presynaptic voltage-gated Ca²⁺
channels; insufficient Ca²⁺ prevents vesicle fusion and
release. (Stahl Ch.1 presynaptic events). Cambridge
University Press & Assessment
• B: Postsynaptic receptor internalization reduces
responsiveness but does not explain failure of presynaptic
release.
• C: Monoamine oxidase is intracellular and in
terminals/mitochondria; it does not act in the cleft to
immediately prevent activity-dependent release.
• D: Postsynaptic second-messenger changes don’t acutely
block presynaptic vesicle fusion.
Teaching Point: Ca²⁺ influx at presynaptic terminals is essential
for neurotransmitter exocytosis.
Citation: Ch. 1, Function: Presynaptic Events. Cambridge
University Press & Assessment
Item 2
Reference: Ch. 1, Space: The Chemically-Addressed Nervous
System
Question Stem: A drug is described as acting by “volume
transmission” rather than synaptic transmission. Which clinical
implication best follows?
,A. The drug’s effects are likely spatially diffuse, affecting many
nearby neurons.
B. The drug will exclusively activate ionotropic receptors.
C. The drug will only act at axo-axonic synapses.
D. The drug cannot influence G protein-coupled receptors.
Correct Answer: A
Rationales:
• A (Correct): Volume transmission refers to extracellular
diffusion of transmitters/neuromodulators across
extracellular space, producing diffuse effects on multiple
targets. (Stahl Ch.1 space). psyberspace.com.au
• B: Ionotropic receptor activation is not required for volume
transmission; both ionotropic and metabotropic receptors
can be influenced.
• C: Axo-axonic synapses are a specific synaptic
arrangement, not synonymous with diffuse volume
transmission.
• D: Metabotropic GPCRs are commonly affected by volume
transmission.
Teaching Point: Volume transmission produces broad
extracellular, rather than point-to-point, signaling.
Citation: Ch. 1, Space: The Chemically-Addressed Nervous
System. psyberspace.com.au
, Item 3
Reference: Ch. 1, Time: Fast-Onset versus Slow-Onset Signals
Question Stem: A clinician chooses a benzodiazepine for acute
anxiety but prescribes an SSRI for long-term management.
Which explanation best matches the pharmacologic difference?
A. Benzodiazepines enhance fast ionotropic GABA-A signaling
(rapid onset); SSRIs act indirectly leading to slow adaptive
changes.
B. Benzodiazepines increase monoamine synthesis; SSRIs
directly activate ion channels.
C. Benzodiazepines degrade neuropeptides quickly; SSRIs inhibit
synaptic vesicle release.
D. Both drugs act with identical onset but different side-effect
profiles.
Correct Answer: A
Rationales:
• A (Correct): Benzodiazepines are positive allosteric
modulators of GABA-A ionotropic receptors producing
rapid anxiolysis; SSRIs alter serotonin levels and induce
slower synaptic and gene-expression changes. (Stahl Ch.1
time; fast vs slow). Cambridge University Press &
Assessment
• B: Benzodiazepines do not increase monoamine synthesis;
SSRIs do not directly activate ion channels.
Neuroscientific Basis and Practical Applications
5th Edition
Author(s)Stephen M. Stahl
TEST BANK
Item 1
Reference: Ch. 1, Function: Presynaptic Events
Question Stem: A patient’s synaptic terminals fail to release
neurotransmitter despite normal action-potential arrival. Which
presynaptic mechanism is the most likely direct cause?
A. Failure of voltage-gated Ca²⁺ channel opening leading to
reduced intracellular Ca²⁺.
B. Increased postsynaptic receptor internalization decreasing
signal detection.
C. Excessive monoamine oxidase activity in the synaptic cleft
degrading neurotransmitter.
D. Upregulation of postsynaptic second-messenger systems
causing negative feedback.
Correct Answer: A
Rationales:
, • A (Correct): Neurotransmitter exocytosis is tightly coupled
to Ca²⁺ influx through presynaptic voltage-gated Ca²⁺
channels; insufficient Ca²⁺ prevents vesicle fusion and
release. (Stahl Ch.1 presynaptic events). Cambridge
University Press & Assessment
• B: Postsynaptic receptor internalization reduces
responsiveness but does not explain failure of presynaptic
release.
• C: Monoamine oxidase is intracellular and in
terminals/mitochondria; it does not act in the cleft to
immediately prevent activity-dependent release.
• D: Postsynaptic second-messenger changes don’t acutely
block presynaptic vesicle fusion.
Teaching Point: Ca²⁺ influx at presynaptic terminals is essential
for neurotransmitter exocytosis.
Citation: Ch. 1, Function: Presynaptic Events. Cambridge
University Press & Assessment
Item 2
Reference: Ch. 1, Space: The Chemically-Addressed Nervous
System
Question Stem: A drug is described as acting by “volume
transmission” rather than synaptic transmission. Which clinical
implication best follows?
,A. The drug’s effects are likely spatially diffuse, affecting many
nearby neurons.
B. The drug will exclusively activate ionotropic receptors.
C. The drug will only act at axo-axonic synapses.
D. The drug cannot influence G protein-coupled receptors.
Correct Answer: A
Rationales:
• A (Correct): Volume transmission refers to extracellular
diffusion of transmitters/neuromodulators across
extracellular space, producing diffuse effects on multiple
targets. (Stahl Ch.1 space). psyberspace.com.au
• B: Ionotropic receptor activation is not required for volume
transmission; both ionotropic and metabotropic receptors
can be influenced.
• C: Axo-axonic synapses are a specific synaptic
arrangement, not synonymous with diffuse volume
transmission.
• D: Metabotropic GPCRs are commonly affected by volume
transmission.
Teaching Point: Volume transmission produces broad
extracellular, rather than point-to-point, signaling.
Citation: Ch. 1, Space: The Chemically-Addressed Nervous
System. psyberspace.com.au
, Item 3
Reference: Ch. 1, Time: Fast-Onset versus Slow-Onset Signals
Question Stem: A clinician chooses a benzodiazepine for acute
anxiety but prescribes an SSRI for long-term management.
Which explanation best matches the pharmacologic difference?
A. Benzodiazepines enhance fast ionotropic GABA-A signaling
(rapid onset); SSRIs act indirectly leading to slow adaptive
changes.
B. Benzodiazepines increase monoamine synthesis; SSRIs
directly activate ion channels.
C. Benzodiazepines degrade neuropeptides quickly; SSRIs inhibit
synaptic vesicle release.
D. Both drugs act with identical onset but different side-effect
profiles.
Correct Answer: A
Rationales:
• A (Correct): Benzodiazepines are positive allosteric
modulators of GABA-A ionotropic receptors producing
rapid anxiolysis; SSRIs alter serotonin levels and induce
slower synaptic and gene-expression changes. (Stahl Ch.1
time; fast vs slow). Cambridge University Press &
Assessment
• B: Benzodiazepines do not increase monoamine synthesis;
SSRIs do not directly activate ion channels.
