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发育性缺氧缺血性损伤后纹状体乙酰胆碱释放的增强药理学刺激。

Augmented pharmacologic stimulation of striatal acetylcholine release following developmental hypoxic-ischemic injury.

作者信息

Oo T F, Naini A, Burke R E

机构信息

Department of Neurology, Columbia University, New York, NY 10032, USA.

出版信息

Brain Res. 1996 Jan 8;706(1):145-50. doi: 10.1016/0006-8993(95)01240-0.

Abstract

We have previously shown that developmental hypoxic-ischemic injury in a unilateral rodent model leads to an increase in both morphologic and biochemical indices of striatal cholinergic neurons. To investigate the functional significance these changes, we have used the in vivo microdialysis technique to examine the regulation of striatal acetylcholine release in awake, adult rats following postnatal hypoxic-ischemic injury. We have found that injury does not alter basal release or acetylcholine, but it results in a marked augmentation in the increase of acetylcholine release normally observed after infusion of atropine or pirenzepine.

摘要

我们先前已经表明,单侧啮齿动物模型中的发育性缺氧缺血性损伤会导致纹状体胆碱能神经元的形态学和生化指标均增加。为了研究这些变化的功能意义,我们使用体内微透析技术来检测出生后缺氧缺血性损伤的成年清醒大鼠纹状体乙酰胆碱释放的调节情况。我们发现,损伤不会改变基础释放或乙酰胆碱,但会导致在注入阿托品或哌仑西平后通常观察到的乙酰胆碱释放增加显著增强。

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