Abstract
A possible cellular basis for dopaminergic sensitization by long-term dopamine mimetics was examined in rat brain striatum. Long-term apomorphine or amphetamine administration (10 mg/kg/day for 14 days) resulted in a decrease in the specific binding of 3H-apomorphine, but no change in 3H-haloperidol binding. Long-term apomorphine treatment also enhanced the cataleptogenic action of haloperidol, wtih many rats being spontaneously cataleptic after apomorphine withdrawal. It is suggested that the reduced 3H-apomorphine binding signifies less presynaptic receptors. This permits less autoregulation and enhanced dopamined agonist action, possibly accounting for the dopaminergic sensitization by long-term agonists.
Published Version
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