depression Flashcards
Which of the following best explains why traditional monoamine antidepressants take weeks to show clinical effects?
A) They require time to increase monoamine neurotransmitter levels in the brain.
B) The delay is due to the time it takes for neuroplastic changes, such as synapse remodeling, to occur.
C) Monoamine transporters must first be degraded before the drugs can have an effect.
D) The body needs to metabolize and eliminate excess neurotransmitters before homeostasis is achieved.
Monoamine-based antidepressants (like SSRIs) increase neurotransmitter levels immediately, but their therapeutic effects take weeks. This is because they induce long-term changes like synaptic remodeling and neuroplasticity, rather than just altering neurotransmitter levels.
The limbic brain is primarily responsible for which of the following functions in relation to depression?
A) Regulating motor coordination and voluntary movement.
B) Enhancing sensory processing and memory storage.
C) Processing emotions and motivation, often showing altered activity in depression.
D) Controlling autonomic functions such as heart rate and respiration.
c-the limbic system provides emotional flavour.
how does depression affect the limbic system
it increases limbic areas such as the amygdala and decreases areas in the brain correlating to motivation
changes in brainsize affect nuerotransmitter release and postsynaptic responses
. Why was the discovery of reserpine significant for understanding depression?
A) It was the first drug shown to reduce depressive symptoms by increasing monoamine neurotransmitter levels.
B) It demonstrated that depleting monoamines could induce depressive-like symptoms, supporting the monoamine hypothesis.
C) Reserpine blocked glutamate receptors, showing that glutamatergic signaling plays a key role in mood disorders.
D) It inhibited serotonin synthesis, providing the first evidence that serotonin was involved in depression.
It demonstrated that depleting monoamines could induce depressive-like symptoms, supporting the monoamine hypothesis.
A researcher is studying brain imaging in depressed patients. Which of the following findings would most strongly support the limbic dysfunction hypothesis?
A) Increased activity in the prefrontal cortex and decreased activity in the amygdala.
B) Increased engagement of the amygdala and decreased engagement of the striatum.
C) Enhanced dopamine release in the basal ganglia with reduced serotonin uptake in the hippocampus.
D) Suppressed norepinephrine release across all limbic structures.
Increased engagement of the amygdala and decreased engagement of the striatum.
Which statement best differentiates the glutamate hypothesis from the monoamine hypothesis of depression?
A) The glutamate hypothesis focuses on reduced excitatory signaling, whereas the monoamine hypothesis focuses on neurotransmitter depletion.
B) The glutamate hypothesis proposes that depression is caused by excessive neuronal activation, whereas the monoamine hypothesis suggests serotonin deficiency.
C) The glutamate hypothesis emphasizes long-term neurotransmitter depletion, whereas the monoamine hypothesis is based on rapid neuronal adaptation.
D) The glutamate hypothesis was disproven when MAO inhibitors were found to treat depression effectively.
The glutamate hypothesis focuses on reduced excitatory signaling, whereas the monoamine hypothesis focuses on neurotransmitter depletion.
Ketamine is considered a breakthrough treatment for depression because it:
A) Blocks serotonin and norepinephrine transporters, leading to rapid improvements in mood.
B) Increases dopamine release in the mesolimbic system, restoring motivation and emotional processing.
C) Acts as an NMDA receptor antagonist, triggering glutamate bursts that promote synaptic remodeling.
D) Inhibits monoamine oxidase, preventing the breakdown of key neurotransmitters associated with mood regulation.
Acts as an NMDA receptor antagonist, triggering glutamate bursts that promote synaptic remodeling.
how does ketamine combat depression?
depression decreases glutamatergic signalling in the cortex
ketamine increases glutamate (glutamate burst), which blocks NMDA receptors on GABA internuerons. this burst of glutamate remodels the synapse and reset GABA and glutamate receptors, increasing BDNF and gene transcription
Why is synaptic remodeling considered a key component of successful antidepressant treatment?
A) It enhances neurotransmitter reuptake efficiency, reducing the likelihood of overstimulation.
B) It strengthens neuronal connections, allowing for better emotional regulation and cognitive flexibility.
C) It prevents excessive neurotransmitter degradation, maintaining higher monoamine levels in the synapse.
D) It suppresses limbic system hyperactivity, leading to a reduced stress response.
It strengthens neuronal connections, allowing for better emotional regulation and cognitive flexibility.
Which of the following best explains why psychedelics like psilocybin are being explored as potential antidepressants?
A) They selectively inhibit serotonin reuptake, leading to long-lasting mood elevation.
B) They bind to BDNF receptors, enhancing neuroplasticity and resetting cortical networks.
C) They block norepinephrine transporters, increasing motivation and reducing fatigue.
D) They suppress amygdala hyperactivity, eliminating emotional responses associated with depression.
They bind to BDNF receptors, enhancing neuroplasticity and resetting cortical networks.
patient taking an MAO inhibitor eats a meal rich in aged cheese. What is the most likely physiological consequence?
A) An acute hypertensive crisis due to excess tyramine binding to adrenergic receptors.
B) A rapid increase in serotonin levels leading to serotonin syndrome.
C) Severe sedation due to excessive inhibition of norepinephrine release.
D) A sudden depressive episode caused by excessive neurotransmitter breakdown.
An acute hypertensive crisis due to excess tyramine binding to adrenergic receptors.
tyramine acts like a noradrenaline (sympathiomimetic monoamine) and is degraded by MAO
. Why might traditional SSRIs fail to be effective in some patients with depression?
A) Some forms of depression may not be caused by serotonin depletion but rather by glutamate system dysfunction.
B) SSRIs increase serotonin levels immediately, but serotonin receptors in the brain do not respond to these changes.
C) The body develops tolerance to SSRIs within the first few days of treatment, making them ineffective long-term.
D) SSRIs suppress dopamine and norepinephrine release, worsening symptoms of anhedonia and fatigue.
Not all cases of depression are due to low serotonin levels—some may involve glutamatergic dysfunction. This explains why SSRIs help some but not all patients, leading to the search for alternative treatments like ketamine.
Brain-Derived Neurotrophic Factor (BDNF) is essential for which of the following processes in relation to depression?
A) Breaking down excess neurotransmitters to prevent overstimulation.
B) Promoting neuroplasticity by supporting synaptic growth and neuronal survival.
C) Blocking NMDA receptors to regulate glutamate release.
D) Inhibiting serotonin reuptake to increase synaptic serotonin levels.
: BDNF is a key neurotrophic factor that supports neuron survival, synapse formation, and brain plasticity. Low BDNF levels are associated with depression, and treatments like ketamine and psychedelics may work by increasing BDNF and promoting synaptic remodeling.
what is the difference between SSRI’s and SNRI’s?
SSRI’s are selective serotonin reuptake inhibitors. selective for serotonin transporters and bind to BDNF receptors (TRKB)
SNRI’s are serotonin norephinephrine reuptake inhibitors.
Ipronazid, is an example of a….
monoamine inhibitor
how do reserpine and iproniazia work differently?
reserpine: lowers dopamine and norephinephrine
iproniazia: is a monoamine oxidaseinhibiter, increases the concentration of monamine in the synapse, increasing response in the brain
fluoxetine and Prozac are examples of….
serotonin norephinephrine transporter inhibitors
