Flashcards in Week 6 Deck (81)
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1
Affective Disorders
disorders of MOOD (depression & mania)
2
Depressed mood symptoms
1. profound changes in activity (increase or decrease)
2. changes in sleep (insomnia or hypersomnia)
3. suicidal ideation or thoughts of death
3
Mania symptoms
-feelings of grandiosity
-excessive talking
-decreased need for sleep
-distractibility
-engaging in risky behavior
4
Areas 25
Frontal Cortex & Cingulate Gyrus
*important in mood disorders
depression = over or under activity
5
Nucleus accumbens and anhydonia
GABA and dynorphin pathway
-decreases VTA activity
-->decreased reinforcement
-->decreased pleasure
6
Iproniazid origins
used to treat TB originally
-increased mood to point of euphoria
7
Reserpine origins
when hypertensive patients given reserpine
caused depression
8
Chlorpromazine origin
antihistamine that had antipsychotic effects
9
imipramine origin
antidepressant activity
10
iproniazid mechanism
MAO-I (monoamine oxidase inhibitor)
-->enhanced NT functioning
-->elevated mood
11
Reserpine mechanism
binds to vesicles in Monoamine terminals
-->prevents NT from entering/binding
-->decrease NT functioning
-->depressed mood
12
amphetamines mechanisms
increases monoamine functioning in 3 ways
1. blocks reuptake of all 3 monoamines
-->NTs stay in synapse longer
2. enhances release of monoamines
*probably due to MAO-I activity (package more NT)
3. directly stimulate post-synaptic receptors
13
Raphe nucleus projections
*unilateral
projects to:
-hypothalamus
-thalamus
-hippocampus
-MFB
14
Locus Coeruleus projections
*unilateral
projects to:
-hypothalamus
-amygdala
-hippocampus
15
Monoamine pathways tend to be...
unilateral
16
5HT-1A receptor locations
cerebral cortex
hippocampus
septum
amygdala
raphe nucleus
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5HT-2A receptor locations
cerebral cortex & basal ganglia
18
5HT-2C receptor locations
hippocampus, cerebral cortex
19
NE receptor locations
hippocampus
cerebral cortex
20
Ways drugs can change neural activity
1. alter synthesis
2. interfere with vesicle storage
3. directly stimulate receptors
4. block enzyme breakdown of NT (MAO-I's)
5. interfere with reuptake
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1st generational antidepressants (traditional)
-TCA's
-MAO-I
-lithium
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Atypical antidepressants (newer)
-SSRI
-SNRI
-Buproprion
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TCA
some block/hamper reuptake of NE more efficiently than they block reuptake of serotonin
others block reuptake of serotonin more efficiently than they block reuptake of NE
24
MAO-I
inhibit MAO enzyme
-->more NT packaged
-->release of more NT molecules with each AP
25
SSRI
block reuptake of serotonin
very little blocking of NE
26
SNRI
serotonin and NE reuptake inhibitors
27
buproprion
blocks reuptake of DA (and NE)
28
Monoamine theory of affective disorders
disorders are result of underactive monoamine systems in the brain
OR levels of monoamine molecules are too low
29
failure of monoamine theory of affective disorders
fails to explain why there is a 10-14 delay from onset of meds to clinical improvements
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