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长期给予氯米帕明可逆转NMDA诱发的中缝核多巴胺释放减少。

Chronic clomipramine administration reverses NMDA-evoked decreases in dopamine release in the raphe nuclei.

作者信息

Pallotta M, Segieth J, Whitton P S

机构信息

Istituti Di Farmacologia i Tossicologia, Facolta Di Medicina E Chirugia, Universita Degli Studi Di Napoli 'Frederico II', Via Constantinaopli 16, 80138, Naples, Italy.

出版信息

Brain Res. 1999 Mar 27;823(1-2):217-20. doi: 10.1016/s0006-8993(99)01174-9.

DOI:10.1016/s0006-8993(99)01174-9
PMID:10095031
Abstract

The effect of acute or chronic treatment with the antidepressant clomipramine (CIM) on basal and N-methyl-d-aspartate (NMDA) evoked release of dopamine (DA) in rat raphe has been studied using microdialysis. Acute injection of CIM (10 or 20 mg/kg) caused a decrease in raphe DA release, as did infusion of NMDA (25-100 microM) into this region. When NMDA infusion was preceded by a single acute injection of CIM no differences between NMDA and NMDA plus CIM treated groups was observed. Chronic (15 day) treatment with CIM caused a dose-dependent increase in basal extracellular DA. In addition the effect of infusing NMDA into the raphe on DA release was markedly reduced or abolished. This suggests that adaptive changes occur in NMDA receptor function during treatment with CIM.

摘要

使用微透析技术研究了抗抑郁药氯米帕明(CIM)急性或慢性治疗对大鼠中缝核基础状态下及N-甲基-D-天冬氨酸(NMDA)诱发的多巴胺(DA)释放的影响。急性注射CIM(10或20 mg/kg)导致中缝核DA释放减少,向该区域注入NMDA(25 - 100 microM)时也出现这种情况。当在注入NMDA之前单次急性注射CIM时,未观察到NMDA处理组与NMDA加CIM处理组之间存在差异。CIM慢性(15天)治疗导致基础细胞外DA呈剂量依赖性增加。此外,向中缝核注入NMDA对DA释放的影响明显减弱或消除。这表明在CIM治疗期间NMDA受体功能发生了适应性变化。

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