Matsubara K
Eur J Pharmacol. 1986 Feb 18;121(2):297-301. doi: 10.1016/0014-2999(86)90505-4.
The involvement of beta-endorphin (beta-END) in the long-lasting antagonistic effect of caerulein (CLN) on amphetamine (AMP) hyperactivity in rats was investigated. Injection of beta-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 beta-END synthesis. These findings indicate that beta-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 receptors activated by beta-END.
研究了β-内啡肽（β-END）在蛙皮素（CLN）对大鼠苯丙胺（AMP）所致活动亢进的持久拮抗作用中的参与情况。向侧脑室或伏隔核注射β-END抗血清可消除CLN的作用，而注射正常兔血清对AMP敏感性在约2周内无影响，这与完整大鼠的情况相同。此外，长期地塞米松治疗可阻断CLN的作用，因为地塞米松可抑制β-END的合成。这些发现表明，伏隔核中的β-END在产生对CLN的持久作用中起重要作用，提示β-END激活的阿片受体在突触前抑制了AMP诱导的伏隔核中多巴胺的释放。
