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Biological explanation for schizophrenia: Dopamine hypothesis (Post…
Biological explanation for schizophrenia:
Dopamine hypothesis
Post mortems
Post mortems
Falkai et al (1988)
Autopsies found people with schizophrenia have larger than usual number of dopamine receptors
Increase of DA in brain structures and receptor density
DA production is abnormal for schizophrenia
Recent research
Seeman (2013)
Schizophrenics may have higher number of DA receptors - 6% increase
These receptors have a higher infinity to dopamine, they're more likely to bind to the neurotransmitter when it is present in the synapse
A biochemical explanation of schizophrenia, suggests an excess of the neurotransmitter dopamine may be responsible for schizophrenia.
Evidence comes from drug studies, post mortems, pet scans and animal studies
Dopamine increase in the
mesolimbic pathway -> positive symptoms
Dopamine increase in the
mesocortical pathway -> negative symptoms
PET scans and animal studies
PET scans
Lindstroem et al (1999)
L-Dopa (radioactively labelled chemical) given to 10 schizophrenics and 10 with no diagnosis
Taken up quicker with schizophrenic patients, receptors more sensitive to the drug
They produced more DA than the control group
Animal studies
Randrup and Munkvad (1966)
Raised dopamine levels of rats by injecting them with amphetamine
Change in behaviour, more stereotyped, aggressive and isolated
Resulted in psychotic behaviour characteristics of schizophrenics
This research sparked the dopamine hypothesis
Evaluation
Strengths
1. Amphetamines produce symptoms similar to those of excess dopamine
Some evidence comes from effects of drugs such as amphetamines causing excess dopamine, resulting in symptoms of psychosis, which are similar to positive symptoms of schizophrenia
But excess dopamine has a stimulant effect (e.g overconfidence and high alertness), which are symptoms of mania rather than schizophrenia
2. People with schizophrenia are more sensitive to dopamine uptake
Scanning shows if those with schizophrenia are given amphetamines there is a greater release of dopamine than if people without schizophrenia are given the drug
Suggests those with schizophrenia are more sensitive to excess dopamine than others
Carlsson (2000)
3. Phenothiazines block dopamine receptors and reduce schizophrenic symptoms
A group of drugs including chlorpromazine, given to people with schizophrenia
Alleviates symptoms and block dopamine receptors
If receptors are blocked, less dopamine will be taken up so the effects of excess dopamine are avoided
Weaknesses
1. PET scans show blocking dopamine receptors doesn't always remove symptoms
Drugs that block dopamine don't reduce schizophrenia symptoms who have had the illness for 10 years + (even if the block is 90% effective)
2. Blocking dopamine receptors takes a few days work
Anti-schizophrenic drugs block the dopamine receptors almost immediately but calming effects aren't noticed for several days
Suggests something other than excess dopamine causes psychotic symptoms
3. Social and environmental factors are involved
Seem to trigger schizophrenia, so a biological explanation isn't sufficient
Perhaps stressful events in life may trigger production of excess dopamine
Link between social class and schizophrenia --> third explanation