AO3 - Dopamine Hypothesis Schizophrenia

• The dopamine hypothesis has generated huge amounts of research and driven drug treatments that have had success in treating people with schizophrenia.
• As demonstrated by Lindstroem et al (1999) it is now possible to indirectly measure dopamine levels through scanning techniques, for example using radio labelled L-DOPA to compare healthy people with those with schizophrenia.
• Support for the dopamine hypothesis comes from the evidence in drug therapy. Antipsychotic drugs reduce dopamine activity and also reduce the intensity of symptoms (Tauscher et al, 2014).
• Curran et al (2004) found that amphetamines increase dopamine activity and worsen symptoms in people with schizophrenia.
• Tenn et al (2003) supports the dopamine hypothesis after inducing schizophrenia like symptoms in rats using amphetamines. They then relieved the symptoms using drugs that reduce dopamine activity.
• The dopamine hypothesis has been criticised for being too simplistic and inconclusive. Excess dopamine has been associated with the positive symptoms of schizophrenia but does not explain the negative symptoms.
• Healy (2000) suggested that drug companies have a vested interest in promoting the dopamine hypothesis because they stand to make huge profits from antipsychotics.
• Davis et al (1991) suggested that high levels of dopamine are not found in all individuals with schizophrenia.
• One limitation of the dopamine hypothesis is evidence for the central role of glutamate. There is some belief that glutamate levels are lowered in people with schizophrenia (Carlsson et al, 2000).
• McCutcheon et al (2020) suggest that post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with schizophrenia.