Yamada S, Takaki T, Yokoo H, Tanaka M
Institute of Brain Diseases, Kurume University School of Medicine, Japan.
Nihon Shinkei Seishin Yakurigaku Zasshi. 1995 Feb;15(1):43-52.
Haloperidol-induced changes in evoked dopamine (DA) release from striatal slices in rats were investigated. The dose-response curves for haloperidol to changes in the evoked DA release were found to be biphasic (small doses increased the release and large doses inhibited), which were shifted to the left by longer periods of superfusion with haloperidol. This rapid tolerance or inhibition of haloperidol-induced increases in evoked DA release was reduced or attenuated by the superfusion with acetylcholine (ACh) antagonists or B-HT920 and was enhanced by ACh agonists. The microinjection of kainic acid into the rat striatum 4 days before the experiment reduced the rapid tolerance or inhibition of the haloperidol-induced increase in evoked DA release. These data indicate that intrinsic ACh neurons in the striatum may play an important role in the induction of the rapid tolerance or inhibition of haloperidol-induced increase in evoked DA release from striatal slices in rats.
研究了氟哌啶醇诱导的大鼠纹状体切片中诱发多巴胺（DA）释放的变化。发现氟哌啶醇对诱发DA释放变化的剂量反应曲线呈双相性（小剂量增加释放，大剂量抑制），随着氟哌啶醇长时间灌流，曲线向左移动。乙酰胆碱（ACh）拮抗剂或B-HT920灌流可减少或减弱氟哌啶醇诱导的诱发DA释放增加的快速耐受或抑制，而ACh激动剂则增强这种作用。实验前4天向大鼠纹状体内微量注射 kainic 酸可减少氟哌啶醇诱导的诱发DA释放增加的快速耐受或抑制。这些数据表明，纹状体内的内在ACh神经元可能在氟哌啶醇诱导的大鼠纹状体切片中诱发DA释放增加的快速耐受或抑制的诱导中起重要作用。
