bio explanation of schiz: NT Flashcards

1
Q

what is a NT

A

chemicals released in pre-synaptic neuron into synaptic cleft after an action potential. they stimulate post-synaptic neuron and assist that neuron to create its own action potential. The function is that they allow neurons to communicate and our brains to think and feel and bodies to do things

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2
Q

what is the dopamine hypothesis

A

schizo explained by changes of dopamine functioning in the brain

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3
Q

what is hyperdopaminergia (EXCESS DOPAMINE)

A
  • high levels of dopamine caused by low levels of beta hydroxylase (enzyme) which would break down dopamine= build up in synapses
  • excess n.o of dopamine receptors eg Owen,1978 found via post mortem examinations schizo brains had higher density of dopamine receptors than those not w schizo

-dopamine hypothesis- due to hypersensitive of dopamine receptors (D2)

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4
Q

what is hypodopaminergia? (dopamine deficiency )

A

negative symptoms may also be explained by irregular serotonin activity, as serotonin regulates dopamine in mesolimbic pathway

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5
Q

what is the mesolimbic pathway

A

positive symptoms, excess dopamine activity , delusion/hallucinations

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6
Q

what is mesocortical pathway

A

negative symptoms, not enough dopamine, apathy, lack of self care

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7
Q

applications from theory

A

dev of anti-psychotic drugs more effective at reducing +ve than neg and nasty side effects

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8
Q

methodology +

A

people w schizo more sensitive to dopamine uptake scanning shows if people with schiz given amphetamines greatere release of dopamine than people w/o schiz given amphetamines suggesting they are more sensitive to excess dopamine carlsson et al 2000

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9
Q

methodology -

A

ampthetamines produce only symptoms that are like positce symtopms of schizo which suggests dopamine hypothesis isnt sufficient and doesnt explain neg symptoms

theory cannot prove excess dopamine causes schizophrenia instead it may be a symptom of schizophrenia and having schizophrenia may change brain activity

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10
Q

evidence for

A

zipursky et al 90% effective drug treatments used to treat schizophrenia work by blocking dopamine ( however doesnt lways remove symptoms)

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11
Q

evidence against

A

alpert and friedhoff found patients didn’t improve at all after taking dopamine antagonists, and some medications eg clozapine are effective bocus on other NT eg serotonin

when glutamate production is blocked causes psychotic symptoms eg when people take PCP
reductionist as ignores other factors eg social brown and birely found 50& of schizo patients reported major life event 3 weeks prior relapse so there may be social conditions triggering

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