Modulation of G Proteins in Rat Striatum by Neuroleptic Drugs and a Peptidomimetic Analog of Pro-Leu-Gly-NH2

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: Stimulant-induced psychosis is similar in some ways to schizophrenia;Overmedicated Parkinson′s patients exhibit schizophrenialike symptoms; andThe antipsychotic drugs (neuroleptics) used to treat schizophrenia block dopamine receptors (Grace, 1991; Ellison, 1994; Kane and McGlashan, 1995).