PSYB65H3 Lecture Notes - Lecture 6: Monoamine Oxidase, Dopamine Receptor, Tricyclic Antidepressant

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Published on 18 Nov 2012
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Lecture 6 - Psychiatric Disorders
Schizophrenia
- most patients have auditory hallucinations – ppl talking to them, and delusions – ppl plotting against them
- recent findings show that sch and affective (emotional) disorder like depression share the same genes
- age of onset prior to 30, usually early adulthood
Neuropsychological:
- poor performance in frontal lobe tasks; tests of frontal lobe function
=> issues in the frontal lobes, studies aren’t 100% conclusive
- poor performance on tests of verbal and nonverbal memory
- most other neuropsych tests show completely normal
- most patients have enlarged ventricles and lighter brains
=> may be due to the prescribed tranquilizers that patients have to take for many years
- hard to determine what effects are caused by the actual disease, and what effects are caused due to side effects of
the medication
Genetic:
- 1% of population develops sch, in immediate family 10-15% will develop if a relative has it (parents, children,
siblings)
=> suggests genetic basis
- twin studies show di-zygotic (non-identical) ratio is about 10-15% (same as other family members); monozygotic
(identical) prevalence goes up 40-75%
=> something else at play, since identical twins have identical DNA, should be 100% prevalence
=> other factors alter the prevalence
- twins separated at birth 9 out of 12 cases had sch in both twins => predominantly genetic
Psychopharmacology:
- early work done w anti-histamines – makes ppl drowsy
=> tried w sch patients – first pharmacological tool, in order to attempt to calm patients down
- it was found that drugs that were most effective were all dopamine antagonists
=> most used were phenothiazines, most common being chlorpromazine (most effective)
=> block biogenic amines/monoamines receptor site, effectiveness of the drug were selective dopamine antagonists
– blocking the dopamine receptor
- stimulating dopaminergic system, eg by using amphetamine (ecstasy) resulted in sch symptoms reappearing
- ppl who take amphetamines in high doses over long time show sch symptoms (psychiatrists cant tell them from
real sch patients) => have hallucinations and delusions
*blocking receptors makes ppl better, stimulating receptors makes ppl worse/makes normal ppl appear like sch
- brain tissue showed normal dopamine levels, but # of dopamine receptors (D4 receptor) is 6 times more abundant
=> certain ppl born w more dopamine receptors
- need to be careful w blocking too many receptors => too little dopamine can result in Parkinson’s symptoms
- continuum between Parkinson’s and Schizophrenia
Affective Disorders
1. Depression:
=> used chemicals to reduce blood pressure, eg rhezorpine – causes reduction in monoamines (leak from synaptic
vesicles)
=> patients taking the drug got an induced depression – monoamines related to depression
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