biological explanations for schizophrenia: neural correlates

Question 1

what was the original dopamine hypothesis based on? (seeman 1987)

Answer 1

drugs used to treat schizophrenia (antipsychotics, which reduce DA) caused symptoms similar to those in people with parkinson’s disease, a condition associated with low DA levels

Question 2

describe the original dopamine hypothesis

Answer 2

• SZ due to high levels of DA (hyperdopaminergia) in subcortical areas of the brain
• excess of DA receptors in pathways from subcortex of broca’s area may explain language related symptoms eg. speech poverty, auditory hallucinations
• messages from neurons that transmit dopamine fire too easily / often leads to hallucinations and delusions (positive symptoms)

Question 3

how did davis et al. (1991) update the dopamine hypothesis?

Answer 3

• added cortical hypodopaminergia ie. abnormally low DA in cortex
• low DA in PFC could explain negative cognitive symptoms

Question 4

origins of abnormal DA function (howes et al. 2017)

Answer 4

genetic, environmental and psychological factors can increase vulnerability to cortical hypodopaminergia which leads to subcortical hyperdopaminergia

Question 5

revised dopamine hypothesis: evidence of neural imaging (patel et al. 2010)

Answer 5

• used PET scans to assess dopamine levels in schizophrenic and normal individuals
• found lower levels of dopamine in the dorsolateral PFC of schizophrenic patients compared to their normal controls

Question 6

revised dopamine hypothesis: animal studies (wang and deutch 2008)

Answer 6

• induced dopamine depletion in the PFC of rats
• resulted in cognitive impairment (eg. memory deficits)
• effects were reversed using olanzapine, an atypical antipsychotic drug thought to have benefits on negative symptoms in humans

Question 7

evaluation: research evidence (curran et al 2004)

Answer 7

amphetamines, which increase DA, worsen symptoms in people with schizophrenia and induce symptoms in those without

Question 8

evaluation: research evidence (tauscher et al. 2014)

Answer 8

antipsychotic drugs reduce DA activity and also reduce the intensity of their symptoms

Question 9

evaluation: research evidence (grilly 2002)

Answer 9

some people who suffer from parkinson’s disease, a neurodegenerative disease categorised by low levels of dopamine, who take the drug L-Dopa to raise their dopamine levels have been found to develop schizophrenia type symptoms

Question 10

evaluation: central role of glutamate

Answer 10

• mccutcheon et al. 2020) - post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia
• several candidate genes for schizophrenia are believed to be involved in glutamate production or processing

Question 11

evaluation: amphetamine psychosis (tenn et al. 2003)

Answer 11

• induced schizophrenia-like symptoms in rats using amphetamines (which increase DA levels)
• relieved symptoms using drugs that reduce DA action, which supports the dopamine hypothesis

Question 12

evaluation: amphetamine psychosis (dépatie and lal 2001)

Answer 12

other drugs that increase DA levels (eg. apomorphine) do not cause schizophrenia-like symptoms

Question 13

evaluation: amphetamine psychosis (garson 2017)

Answer 13

challenges the idea that amphetamine psychosis closely mimics schizophrenia

Question 14

evaluation: evidence from treatment (leucht et al. 2013)

Answer 14

• carried out a meta-analysis of 212 studies that had analysed the effectiveness of different antipsychotic drugs compared with a placebo
• all drugs tested were signficantly more effective than placebo in treatment of positive and negative symptoms achieved through the normalisation of dopamine

Question 15

evaluation: inconclusive supporting evidence

Answer 15

• stimulant drugs (eg. cocaine, amphetamine) have been shown to induce schizophrenic episodes, but they also affect many neurotransmitters other than DA
• evidence for DA concentrations in post-mortem brain tissue has either been negative or inconclusive

Question 16

evaluation: limitation of evidence (moncrieff 2009)

Answer 16

other confounding sources of dopamine release (eg. stress, smoking) are rarely considered

Question 17

evaluaition: challenges to dopamine hypothesis (noll 2009)

Answer 17

• strong evidence against original and revised hypotheses
• argues antipsychotic drugs do not alleviate hallucinations and delusions in about 1/3 of people experiencing these problems
• in some people, hallucinations and delusions are present even though dopamine levels are normal
• other neurotransmitter systems may also produce the positive symptoms

Question 18

evaluation: neural correlates of negative symptoms

Answer 18

• activity in the ventral striatum has been linked to the development of avolition
• VS is believed to be particularly involved in the anticipation of a reward for certain actions
• structural abnormality in this area would lead to lack of motivation

Question 19

evaluation: neural correlates of positive symptoms

Answer 19

• reduced activity in the superior temporal and cingulate gyrus have been linked to the development of auditory hallucinations
• patients experiencing auditory hallucinations showed lower activation levels in these areas than controls