Striatal and nucleus accumbens D1/D2 dopamine receptors in neuroleptic catalepsy

Abstract

Haloperidol (2.5–10 μg) injected bilaterally into the ventro-rostral striatum or into the nucleus accumbens induced dose-dependent catalepsy whereas its injection into the dorso-rostral striatum (2.5 μg) was ineffective. Similarly, the specific antagonist of D₁ receptors, SCH 23390 (1–5 μg), injected into the ventro-rostral striatum or nucleus accumbens, as well as the specific antagonist of D₂ receptors, sulpiride, injected into the ventro-rostral striatum (0.02–15 μg) or nucleus accumbens (1–15 μg), induced a dose-dependent catalepsy. Both drugs (SCH 23390 2 μg, sulpiride 0.5 μg) were ineffective when injected into the dorso-rostral striatum. Doses of sulpiride about 100 times lower than those injected into the nucleus accumbens were sufficient to evoke an equipotent catalepsy when injected into the ventro-rostral striatum. However, similar doses of haloperidol and SCH 23390, injected into the ventro-rostral striatum and nucleus accumbens, evoked a similar catalepsy. It is concluded that (1) the catalepsy induced by systemic administration of haloperidol seems to result from the action of this drug on both the ventro-rostral striatum and the nucleus accumbens, (2) both D₁ and D₂ dopamine receptors in the ventro-rostral striatum are involved in the cataleptogenic action of neuroleptics, and (3) in the nucleus accumbens, only D₁ dopamine receptors seem to play an important role in this phenomenon.