Effects of dopamine antagonists on neuronal histamine release in the striatum of rats subjected to acute and chronic treatments with methamphetamine.
Effects of dopamine antagonists on neuronal histamine release in the striatum of rats subjected to acute and chronic treatments with methamphetamine.
复制标题
多巴胺拮抗剂对接受甲基苯丙胺急性和慢性治疗的大鼠纹状体神经元组胺释放的影响。
DOI：
--
复制
发表时间：
1996
期刊：
影响因子：
--
通讯作者：
T. Watanabe
中科院分区：
文献类型：
--
作者：
C. Ito;K. Onodera;E. Sakurai;M. Sato;T. Watanabe
在这项研究中，我们研究了急性和重复给药甲基苯丙胺（METH）后大鼠纹状体神经元组胺（HA）释放的变化。我们研究了多巴胺受体对MET诱导的HA释放的调节以及MET诱导的HA释放与刻板行为之间的关系。急性给予METH（1 mg/kg）60 min后显著增加HA释放。多巴胺D2受体拮抗剂舒必利和氟哌啶醇预处理阻断了甲基苯丙胺诱导的HA释放增加，而多巴胺D1受体拮抗剂SCH 23390预处理则没有。此外，重复给予METH（3 mg/kg）大大增强了METH（1 mg/kg）再激发后60，80，100，120和180 min的METH诱导的HA释放增加。氟哌啶醇和METH重复治疗阻断了METH再激发引起的HA释放增加。在急性和重复给药METH后，在METH诱导的刻板行为减少后，仍然发现METH诱导的HA释放增加。这些结果表明，甲硫氨酸诱导的纹状体HA释放是由多巴胺D2受体控制的，可能在甲硫氨酸诱导的刻板行为中发挥重要的抑制作用。此外，HA神经元系统通过DA神经传递的持续变化可能部分负责MET诱导的行为敏化。
In this study, we examined the changes in neuronal histamine (HA) release in the rat striatum after acute and repeated administration of methamphetamine (METH). We studied the regulation of METH-induced HA release by dopamine receptors and the relationship between METH-induced HA release and stereotyped behavior. Acute administration of METH (1 mg/kg) significantly increased HA release 60 min later. Pretreatments with the dopamine D2 antagonists sulpiride and haloperidol blocked the METH-induced increase of HA release, whereas pretreatment with a dopamine D1 antagonist, SCH23390, did not. Moreover, repeated administration of METH (3 mg/kg) greatly enhanced the METH-induced increase of HA release 60, 80, 100, 120 and 180 min after rechallenge of METH (1 mg/kg). Repeated treatment with haloperidol and METH blocked the increase of HA release induced by the rechallenge of METH. The METH-induced increase of HA release was still found after the METH-induced stereotyped behavior decreased in both acute and repeated administrations of METH. These findings suggest that the METH-induced HA release in the striatum is controlled by dopamine D2 receptors and may play an important inhibitory role in the METH-induced stereotyped behavior. Furthermore, a persistent change in the HA neuron system through DA neurotransmission may be partially responsible for the METH-induced behavioral sensitization.