NEUROBIOLOGY OF MOOD DISORDERS (100 QUESTIONS)
1. Alpha-1 subtype adrenergic receptors:
a) Are located on serotonergic terminals
b) Are located in the sympathetic system where they control urinary retention
c) Signal via stimulation of adenylyl cyclase
d) a and c
Correct Answer: b
Rationale: Alpha-1 adrenergic receptors are Gq-coupled (not Gs), so they do not
stimulate adenylyl cyclase. They are found in the sympathetic nervous system,
including the internal urethral sphincter, where activation promotes urinary
retention.
2. Which of the following disorders is more common in women?
a) Bipolar I disorder
b) Generalized Anxiety Disorder (GAD)
c) Major Depressive Disorder (MDD)
d) All of the above
e) a and b
f) b and c
Correct Answer: f
Rationale: GAD and MDD are ~2× more common in women. Bipolar I has equal
sex prevalence.
3. Which statement(s) is/are true?
a) Suicidal ideation → abnormalities in norepinephrine in vmPFC and amygdala
b) Anhedonia → abnormalities in dopamine in nucleus accumbens
c) Executive dysfunction → abnormalities in serotonin in hypothalamus
,d) All of the above
e) a and b
f) b and c
Correct Answer: b
Rationale: Anhedonia is linked to mesolimbic dopamine. Suicidal ideation involves
serotonin. Executive dysfunction involves prefrontal dopamine/norepinephrine,
not hypothalamic serotonin.
4. Mechanism of action of SARIs (e.g., trazodone):
a) 5HT2A antagonism potentiates 5HT1A-mediated inhibition of glutamate release
b) Disinhibition of 5HT2A/2C on dopamine and norepinephrine release
c) Increase serotonin via alpha-2 antagonism
d) All of the above
e) a and b
f) a and c
Correct Answer: e
Rationale: SARIs block 5HT2A → disinhibits DA/NE (b) and enhances 5HT1A
effects (a). They increase 5HT via SRI, not alpha-2 antagonism.
5. Risk factor for PTSD:
a) 5-HTT short allele
b) Earlier age at trauma
c) Larger hippocampus size
d) All of the above
e) a and b
f) b and c
Correct Answer: e
Rationale: 5-HTT short allele and younger age increase PTSD risk. Smaller (not
larger) hippocampus is a risk factor.
,6. Monoamine receptor hypothesis of depression:
a) Depression caused by absence of a key monoamine receptor
b) SSRI mechanism = down-regulation of 5-HT1D autoreceptors
c) Supported by serotonin rise first in cortex, then raphe
d) None of the above
Correct Answer: d
Rationale: All statements are false. Hypothesis involves postsynaptic receptor
changes, not absence. SSRI down-regulates 5-HT1A. Serotonin rises first in raphe,
then cortex.
7. BZD binding site on GABA-A receptor involves:
a) Alpha-1 and beta-2
b) Alpha-2 and gamma-2
c) Alpha-1 and beta-1
d) Alpha-1 and alpha-2
Correct Answer: b
Rationale: BZDs bind at alpha (1,2,3,5) and gamma-2 subunit interface.
8. GAD stands for:
a) Generalized anxiety depression
b) Glutamic acid decarboxylase
c) Generalized anxiety disorders
d) All of the above
e) a and b
f) b and c
Correct Answer: f
Rationale: In psychiatry = Generalized Anxiety Disorder. In neurochemistry =
Glutamic Acid Decarboxylase.
, 9. Enzymes found in noradrenergic neurons:
a) Tyrosine hydroxylase
b) Dopamine beta-hydroxylase
c) Monoamine oxidase
d) All of the above
e) b and c
f) None
Correct Answer: d
Rationale: All three enzymes are present: TH (synthesis), DBH (conversion), MAO
(degradation).
10. NOT a symptom of norepinephrine deficiency:
a) Fatigue
b) Slowness of information processing
c) Obsession and compulsion
d) Problem concentrating
Correct Answer: c
Rationale: Obsessions/compulsions are linked to serotonin dysfunction, not NE
deficiency.
11. Classical monoamine hypothesis:
a) Depression caused by absence of monoamine receptors
b) Depression caused by deficiency of monoamines
c) Depression caused by problems in monoamine-activated genes
d) All of the above
Correct Answer: b
Rationale: The classical hypothesis states functional deficiency of monoamines
(5HT, NE, DA).