In order to assess neurotransmitter levels we have to measure the metabolite levels in cerebrospinal fluid.
Are the dopamine discrepancies seen in some people with sz just another symptom of the disease, rather than a cause of it?
Diet and drug use may also seriously affect metabolite levels and results can be difficult to interpret with HVA levels varying widely
Research using PET scans hasn’t been able to detect differences in the dopamine activity of the brains of individuals with sz and those without.
Serotonin has also been identified as a potential influence. Atypical antipsychotics block the D1 receptor and serotonin
Barlow & Durand (1995) - symptoms can be treated with dopamine antagonists (e.g. chlorpromazine).
The Treatment Aetiology Fallacy - just because a treatment works this does not necessarily reveal the cause of the disorder
Kalat (1988) - in most parts of the brain dopamine inhibits glutamate synapses and in others glutamate excites neurones that dopamine inhibits.
High doses of PCP, which inhibits glutamate receptors, produces a much better approximation to schizophrenic symptoms than L-Dopa
Individuals may have a genetic predisposition to dopamine imbalances e.g. Gottesman et al. (1991)
In 2014, it was reported that there were 108 genetic loci associated with sz.
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