Depression

Question 1

depression

Answer 1

mental disorder that impairs social/occupational functioning
14.4%

Question 2

Limbic Brain

Answer 2

cortical barrier between brainstem and cortex
receives ascending information from spinal cord
amygdala
hippocampus
basal ganglia
cingulate gyrus
connections to frontal cortex + hypothalamus

Question 3

fMRI

Answer 3

shows blood oxygen levels in brain
increase in blood-oxygen = increase in neuronal activity
MDD showed increase in limbic system activation and decrease in striatum activation

Question 4

amine hypothesis

Answer 4

monoaminergic neurotransmitters: dopamine norepinephrine, serotonin
modulatory role - mood, arousal, attention
depression is the inadequate monoamine neurotransmission - less NT release, fewer receptors, impaired signal transduction

Question 5

dopamine and NE

Answer 5

synthesis: tyrosine
catalysis: MAO

Question 6

serotonin

Answer 6

synthesis: tryptophan
catalysis: MAO

Question 7

reserpine

Answer 7

antihypertensive drug
depletes dopamine and NE neurons by blocking movement of dopamine into vesicle
causes depression-like syndrome

Question 8

ipronazid

Answer 8

anti-tubercular drug
inhibits monoamine oxidase = increases synaptic concentration of monoamine NTs
alleviates depression

Question 9

problem with amine hypothesis

Answer 9

drugs don’t work in everyone and only work ok
takes weeks to see clinical effects despite immediate effect in the synapse

Question 10

glutamatergic hypothesis

Answer 10

depression is caused by reduced glutamatergic signalling in the cortex
decreased glutamate signalling impacts excitatory and inhibitory function
affects long-term potentiation, neurotrophic production, synapse formation, and gene transcription

Question 11

monoamine targeting antidepressants

Answer 11

MAO inhibitors - block NT breakdown = higher levels in synapse
SSRIs and SNRIs - inhibit serotonin and NE transporters = higher levels in synapse
side effects = nausea, dizziness, weight loss

Question 12

glutamate targeting antagonists

Answer 12

ketamine: non-competitve NMDA receptor antagonist
causes transient burst of glutamate from blocking of NMDA on GABA (can’t bind = build up) → reset of glutamate and GABA systems
narrow therapeutic window + intravenous administration

Question 13

psychedelics

Answer 13

emerging therapy
study - blinding is impossible (placebo) + serious side effects
antidepressant effect by synaptic remodelling via intracelullar 5-HT2a receptors
lipophilic drug crosses membrane to stimulate population of receptors inside cortical neurons = neuronal growth