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The hypothesis that neurochemical abnormalities are involved in schizophrenia
has a long history (Andreasen 1995). However, empirical evidence was provided
only when the mode of action of antipsychotic drugs was shown to be related
to catecholamine metabolism in the brain, and more specifically to blocking
the effect of these drugs on the catecholamine postsynaptic receptors
(Carlsson and Lindkvist 1963). Subsequent research indicated that it was
the capacity of antipsychotics to block the dopamine-2(D2) receptors that
was responsible for their clinical efficacy (Peroutka and Snyder 1980).
Dopamine increases the sensitivity of brain cells to stimuli. Ordinarily,
this heightened sensitivity is useful in increasing a person's awareness
in times of stress or danger. However, for a person with schizophrenia,
the addition of dopamine's effect to an already hyperactive brain state
may tip that person into a psychosis.
Both these mechanisms have been extensively investigated in schizophrenia,
but conclusive evidence in favour of either is thus far lacking. Studies
of dopamine turn-over in patients' body fluids as well as direct determination
of dopamine levels in postmortem brain tissue have yielded conflicting
results (Heritch 1990; Hirsch and Weinberger 1995; Bloom and Kupfer 1995).