Dopamine is the archetypal late '60s, early '70s transmitter, famous for it's involvement in schizophrenia. Like much else from this era, the dopamine story is discovered anew by successive generations. That story – that the dramatic symptoms of schizophrenia are caused by too much dopamine – has survived as fashions have come and gone.

Dopamine is synthesised in pre-synaptic boutons from the amino-acid tyrosine (TYR), via DOPA. Patients who respond well to anti-psychotics appear to have increased synthesis of dopamine (DA).

A recent paper from researchers in London adds a new twist. It appears that those patients who respond well to anti-psychotic drugs (which block dopamine receptors) have elevated pre-synaptic dopamine. In contrast, the (thankfully small) group of patients who don't do so well on anti-psychotics appear to be no different from healthy controls in regard to pre-synaptic dopamine.

Further work, including replication of the findings, will be necessary. But these results suggest that there are dopamine and non-dopamine forms of psychosis.

Hopefully, in time, there will be technological improvements allowing prospective testing of individual patients prior to initiating drug therapy. New, non-dopamine based anti-psychotics are also a priority.

The abstract can be read here

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