Theories of Depression-Craviso Flashcards
What are the areas of the brain involved in the regulation of mood, emotional expression, reward processing, attention, motivation, stress etc?
hypothalamus hippocampus cingulate gyrus amygdala prefrontal cortex ventral striatum
Which neuroimaging techniques have been used to study depression?
PET SCAN: looks at blood flow, tissue metabolism
MRI
**post-mortem–analyze number of cells in a depressed person’s brain
Actual diagnosis: MSE or DSMV
What happens to the gray matter volume & cell counts in the following areas of the brain in a depressed individual? hippocampus cingulate gyrus amygdala prefrontal cortex ventral striatum
all go down!
Except: gray matter volume in the amygdala can go up or down
What is interesting about the blood flow in the brain of a depressed person?
increased blood flow to the amygdala & the prefrontal cortex in a depressed person
What is interesting about the metabolism in the brain of a depressed person, according to PET scans?
increased metabolism int he anterior cingulate cortex in transiently sad normal people & depressed individuals.
After antidepressants, normal metabolism in ACC again.
Individuals who were depressed & showed increased metabolism in the ________ showed a better response to what?
rostral anterior cingulate cortex
better response to antidepressants
In the 1950s…physicians started to form theories of depression based on the action of 2 drugs. Explain.
Reserpine: for HTN induced depression. Depletes neuronal stores of biogenic amines.
Iproniazid: for TB, elevated mood
Inhibits monoamine oxidase.
What is the monoamine hypothesis of depression?
caused by dysfunction of monoamine neurotransmitter systems
mainly serotonin, norepinephrine
also dopamine
How do patients respond to antidepressants? How has this changed the theories of depression?
60-70% have short term response
50% have total remission
time lapse of several weeks before there is an effect
adaptive changes in CNS, not just NT
What is the neurotrophic hypothesis of depression?
depression associated with loss of neurotrophic support
therapy increases neurogenesis & synaptic connectivity in cortical areas like the hippocampus
Why would the neurotrophic hypothesis of depression suggest that antidepressants are effective?
they cause a slow increase in BDNF
this is known to help in neural plasticity, resilience, neurogenesis
synaptogenesis
How are stress & depression interrelated?
hippocampus:
atrophy of neurons b/c of super high cortisol levels
death of neurons w/ severe & prolonged stress
decrease of BDNF
How does long term potentiation relate to treatment of depression?
LTP increases sensitivity of post synaptic neurons to glutamate
NMDA receptor opens & recruits more AMPA receptors to the surface
**goal: get LTP to happen faster w/ antidepressants
Does ketamine help depression?
maybe! and quickly
NMDA glutamate receptor antagonist-binds inside the ion channel
**good for patients who don’t respond to other treatments
effects last days to weeks
Why does ketamine work even tho it is a glutamate antagonist?
we don’t know.
but it increases neurogenesis rapidly
