Affective Disorders

Question 1

How do Monoamine Oxidase Inhibitors [Iproniazid] work?

Answer 1

Inside axonal ending, destroys MAO so it can’t destroy neurotransmitters - agonistic. Very small error margin [danerous]

Question 2

How do reuptake inhibitors work?

Answer 2

Increase transmitter substance in synaptic cleft [agonist]

Question 3

What are common reuptake inhibitors?

Answer 3

tricyclics [work with dopamine, seratonin, norepinephrine]
SSRI - seratonin [Prozac]
SNRI - seratonin &/or norepinephrine inhibitors

Question 4

What is ketamine?

Answer 4

NMDA antagonist [reduces glutamate transmission]

Question 5

What is the primary neurotransmitter?

Answer 5

acetylcholine

Question 6

What is the enzyme that destroys acetylcholine?

Answer 6

acetylcholinesterase

Question 7

What do MAO inhibitors inactivate?

Answer 7

Acetylcholinesterase [agonistic]

Question 8

What does cocaine do?

Answer 8

Inhibit reuptake of dopamine [agonist]

Question 9

What does ketamine do, long term?

Answer 9

produce schizophrenia-like symptoms

Question 10

What are brain stimulation techniques used for depression?

Answer 10

ECT, TMS, deep brain stimulation of subgenual anterior cingulate cortex, stimulate vagus nerve

Question 11

Why is vagus nerve important?

Answer 11

descends into PNS - stimulation reduces depressive effects

Question 12

What is monoamine hypothesis of depression?

Answer 12

Depression results from reduced activity of brain monoamines

Question 13

What is evidence for monoamine hypothesis of depression?

Answer 13

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

Question 14

What is tryptophan?

Answer 14

precursor to seratonin

Question 15

What were effects of tryptophan depletion [lowering brain serotonin] and catecholamine depletion on symptoms of patients receiving SSRI or NERI [norepinephrine reuptake inhibitor?

Answer 15

SSRI patients relapsed when serotonin depleted; NERI patients relapsed when catecholamine depleted
Therefore two types of depression patients

Question 16

What are problems with monoamine depletion theory?

Answer 16

Antidepressant meds take two weeks to work

Depletion procedure only has depressant effect in people with personal or family history [those with risk factors]

Question 17

What is tentative evidence for brain abnormalities?

Answer 17

• 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

Question 18

What is the 5-HT transporter

Answer 18

reuptake mechanism for serotonin

Question 19

What does short allele in 5-HT transporter gene indicate?

Answer 19

pathological; impairs re-uptake, increasing availability of serotonin in the synapse

Question 20

What does possession of one or two short alleles predispose to?

Answer 20

depression

Question 21

How might short alleles predispose to depression?

Answer 21

influences over prenatal development, esp in amygdala and subgenual ACC

Question 22

What do REM sleep patterns in depressed patients show?

Answer 22

Longer REM periods earlier in night

Don’t get slow wave sleep

Question 23

What does REM deprivation do?

Answer 23

Improve mood

Question 24

What do antidepressants do to REM sleep?

Answer 24

Suppress it, increase slow wave sleep

Question 25

What is effect of short REM sleep latency?

Answer 25

increases chance of depression

Question 26

What is effect of living in total darkness on monoaminergic systems?

Answer 26

decreases number of terminal buttons from DA neurons, NE neurons and 5-HT neurons