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1. A limitation is that there is mixed support for the dopamine hypothesis - ✔✔- dopamine agonists like amphetamines increase dopamine levels and make SZ worse, also causing sz-like symptoms in non-sufferers 2. antipsychotics, which act as dopamine antagonists and so reduce dopamine activity, reduce the symptoms of SZ, suggesting that dopamine has a key role in its development, in line with the predictions of the dopamine hypothesis. 3. -On the other hand, some researchers such as Moghaddam and Javitt (2012) have criticised the dopamine hypothesis and biological explanations of SZ as emphasising the role of dopamine too far. 4. For example, the neurotransmitters glutamate and serotonin may also play a key role, as evidenced by the antipsychotic Clozapine acting upon both of these substances and being more effective than other atypical antipsychotics in reducing SZ symptoms
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21.Genetic basis: schizophrenia runs in families - ✔✔there is a strong relationship between genetic similarity of family members and the likelihood of both developing schizophrenia. 22.Gotteman (1991) completed a large-scale family study and found MZ twins have a 48% shared risk of schizophrenia. DZ twins have a shared 50% risk and siblings (about 50% genes shared) have a 9% shared risk. 23.This provides evidence of a genetic basis but also suggests there must be environmental factors too. 24.Neural correlates: brain activity linked with symptoms - ✔✔Neural correlates are measurements of the structure or function of the brain that correlate with the positive or negative symtpons of schizophrenia. 25.Neural correlates: NEGATIVE SYMPTOMS - ✔✔Ventral striatum is involved in anticipations of reward (related to motivation). 26.Loss of motivation (avolition) in schizophrenia may be explained by low activity levels here. 27.Juckel et al. (2006) found a negative correlation between ventral striatum activity and overall negative symptoms. 28.Neural correlates: POSITIVE SYMPTOMS - ✔✔Positive symptoms also have neural correlations
29.Allen et al. (2007) found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus.