Modulation of G Proteins in Rat Striatum by Neuroleptic Drugs and a Peptidomimetic Analog of Pro-Leu-Gly-NH2
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Although the dopamine hypothesis of schizophrenia has gained wide acceptance, it has recently become clear that it requires revision (Seeman and Niznik, 1990 ; Ellison, 1994 ; Kahn and Davis, 1995 ). The original hypothesis asserts that schizophrenia is produced by a hyperdopaminergic state, which exists within central dopaminergic neurons, namely, the mesolimbic and mesocortical (A9 and A10) neurons. This hypothesis is supported by several observations:
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Stimulant-induced psychosis is similar in some ways to schizophrenia;
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Overmedicated Parkinson′s patients exhibit schizophrenialike symptoms; and
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The antipsychotic drugs (neuroleptics) used to treat schizophrenia block dopamine receptors (Grace, 1991 ; Ellison, 1994 ; Kane and McGlashan, 1995 ).
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