Affective Disorders Flashcards
How do Monoamine Oxidase Inhibitors [Iproniazid] work?
Inside axonal ending, destroys MAO so it can’t destroy neurotransmitters - agonistic. Very small error margin [danerous]
How do reuptake inhibitors work?
Increase transmitter substance in synaptic cleft [agonist]
What are common reuptake inhibitors?
tricyclics [work with dopamine, seratonin, norepinephrine]
SSRI - seratonin [Prozac]
SNRI - seratonin &/or norepinephrine inhibitors
What is ketamine?
NMDA antagonist [reduces glutamate transmission]
What is the primary neurotransmitter?
acetylcholine
What is the enzyme that destroys acetylcholine?
acetylcholinesterase
What do MAO inhibitors inactivate?
Acetylcholinesterase [agonistic]
What does cocaine do?
Inhibit reuptake of dopamine [agonist]
What does ketamine do, long term?
produce schizophrenia-like symptoms
What are brain stimulation techniques used for depression?
ECT, TMS, deep brain stimulation of subgenual anterior cingulate cortex, stimulate vagus nerve
Why is vagus nerve important?
descends into PNS - stimulation reduces depressive effects
What is monoamine hypothesis of depression?
Depression results from reduced activity of brain monoamines
What is evidence for monoamine hypothesis of depression?
Reserpine prevents storage of NT in vescicles –> depletion of monoamines –> depression
Suicidal depression related to low level of 5-HIAA [metabolised seratonin]
Antidepressants increase NE or 5-HT [by blocking monoamine reuptake]
Tryptophan deletion procedure - reduces 5-HT levels, reinstates depression in former depressed patients
What is tryptophan?
precursor to seratonin
What were effects of tryptophan depletion [lowering brain serotonin] and catecholamine depletion on symptoms of patients receiving SSRI or NERI [norepinephrine reuptake inhibitor?
SSRI patients relapsed when serotonin depleted; NERI patients relapsed when catecholamine depleted
Therefore two types of depression patients
What are problems with monoamine depletion theory?
Antidepressant meds take two weeks to work
Depletion procedure only has depressant effect in people with personal or family history [those with risk factors]
What is tentative evidence for brain abnormalities?
- decreased levelts of neurotrophic factor
- enlarged ventricles; decreased hippocampal volume
- high levels of activity in amygdala and medial orbital prefrontal cortex
- high levels of activity in subgenual ACC; decreased activity in other frontal areas
- silent cerebral infarctions
What is the 5-HT transporter
reuptake mechanism for serotonin
What does short allele in 5-HT transporter gene indicate?
pathological; impairs re-uptake, increasing availability of serotonin in the synapse
What does possession of one or two short alleles predispose to?
depression
How might short alleles predispose to depression?
influences over prenatal development, esp in amygdala and subgenual ACC
What do REM sleep patterns in depressed patients show?
Longer REM periods earlier in night
Don’t get slow wave sleep
What does REM deprivation do?
Improve mood
What do antidepressants do to REM sleep?
Suppress it, increase slow wave sleep
What is effect of short REM sleep latency?
increases chance of depression
What is effect of living in total darkness on monoaminergic systems?
decreases number of terminal buttons from DA neurons, NE neurons and 5-HT neurons
