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阿片类药物依赖大鼠戒断诱导的蓝斑神经元激活:巨细胞旁核损伤的减弱作用

Withdrawal-induced activation of locus coeruleus neurons in opiate-dependent rats: attenuation by lesions of the nucleus paragigantocellularis.

作者信息

Rasmussen K, Aghajanian G K

机构信息

Department of Psychiatry, Yale University School of Medicine, New Haven, CT.

出版信息

Brain Res. 1989 Dec 29;505(2):346-50. doi: 10.1016/0006-8993(89)91466-2.

DOI:10.1016/0006-8993(89)91466-2
PMID:2598056
Abstract

Single unit activity was recorded in the locus coeruleus (LC) of anesthetized, morphine-dependent rats during naltrexone-precipitated withdrawal. As has been reported previously, LC neurons displayed a strong withdrawal-induced activation of firing rate. Radio-frequency lesions of the nucleus paragigantocellularis (PGi), a major LC afferent, greatly attenuated withdrawal-induced activation of neurons in the LC ipsilateral but not contralateral to the PGi lesion. Lesions of the prepositus hypoglossi, another major LC afferent, did not prevent the withdrawal-induced activation of LC neurons. Kynurenic acid, a non-selective excitatory amino acid antagonist known to block PGi-induced excitations of LC neurons, also blocked the withdrawal-induced activation of LC neurons. These studies indicate that withdrawal-induced activation of the LC in opiate-dependent rats is mediated at least in part by afferents from the PGi which utilize an excitatory amino acid transmitter.

摘要

在纳曲酮诱发的戒断过程中,记录了麻醉的吗啡依赖大鼠蓝斑(LC)中的单单位活动。如先前报道,LC神经元在戒断时表现出强烈的放电率激活。巨细胞旁核(PGi)是LC的主要传入神经,对其进行射频损毁可显著减弱同侧而非对侧LC神经元的戒断诱发激活。舌下前置核是LC的另一个主要传入神经,对其进行损毁并不能阻止LC神经元的戒断诱发激活。犬尿氨酸是一种非选择性兴奋性氨基酸拮抗剂,已知可阻断PGi诱导的LC神经元兴奋,它也能阻断戒断诱导的LC神经元激活。这些研究表明,阿片类药物依赖大鼠中戒断诱导的LC激活至少部分是由PGi的传入神经介导的,这些传入神经利用兴奋性氨基酸递质。

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