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尼古丁引起的蓝斑核神经元兴奋是通过兴奋性氨基酸的释放介导的。

Nicotine induced excitation of locus coeruleus neurons is mediated via release of excitatory amino acids.

作者信息

Engberg G

机构信息

Department of Pharmacology, University of Göteborg, Sweden.

出版信息

Life Sci. 1989;44(21):1535-40. doi: 10.1016/0024-3205(89)90446-3.

DOI:10.1016/0024-3205(89)90446-3
PMID:2567481
Abstract

Previous electrophysiological studies have shown that systemically administered nicotine in low doses increases the firing rate of rat locus coeruleus (LC) neurons. In the present study, this action of nicotine was found to be prevented by pretreatment with kynurenic acid (1 mumol; i.c.v.). In addition, pretreatment with MK 801 effectively blocked the nicotine induced LC excitation in most neurons tested (60%) whereas the rest were left unaffected by this treatment. It is suggested that excitatory amino acids (EAA), e.g. released from nerve terminals from nucleus paragigantocellularis (PGi), indirectly mediated the effect of nicotine on LC neurons.

摘要

先前的电生理研究表明，低剂量全身给药尼古丁可提高大鼠蓝斑（LC）神经元的放电率。在本研究中，发现犬尿烯酸（1 μmol；脑室内注射）预处理可阻止尼古丁的这一作用。此外，MK 801预处理有效阻断了大多数受试神经元（60%）中尼古丁诱导的LC兴奋，而其余神经元则不受该处理影响。提示兴奋性氨基酸（EAA），如从巨细胞旁核（PGi）神经末梢释放的EAA，间接介导了尼古丁对LC神经元的作用。

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