Abstract
The involvement of β-endorphin (β-END) in the long-lasting antagonistic effect of caerulein (CLN) on amphetamine (AMP) hyperactivity in rats was investigated. Injection of β-END antiserum into the lateral ventricle or the nucleus accumbens abolished the CLN effect, whereas the injection of normal rabbit serum had no effect on the susceptibility to AMP for about 2 weeks, as observed in intact rats. Moreover, the CLN effect was blocked by long-term dexamethasone treatment, which inhibits β-END synthesis. These findings indicate that β-END in the nucleus accumbens plays an important role in producing the long-lasting effect on CLN, suggesting that dopamine release induced by AMP in the nucleus accumbens is presynaptically inhibited by opiate receptor activated by β-END.
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