豚鼠海马中内源性阿片对去甲肾上腺素释放的调节

Endogenous opioid regulation of norepinephrine release in guinea pig hippocampus.

作者信息

Simmons M L, Wagner J J, Caudle R M, Chavkin C

机构信息

Department of Pharmacology, University of Washington, Seattle 98195.

出版信息

Neurosci Lett. 1992 Jul 6;141(1):84-8. doi: 10.1016/0304-3940(92)90340-d.

DOI:10.1016/0304-3940(92)90340-d

PMID:1508405

Abstract

Release of endogenous norepinephrine was detected in guinea pig hippocampal slices using a radioligand displacement assay. Focal electrical stimulation released endogenous norepinephrine and caused a calcium-dependent reduction in specific [3H]propranolol binding at beta-adrenergic receptors in the brain slice. The mu-opioid agonist PL017 decreased norepinephrine release, and the inhibition by PL017 could be blocked by the opioid antagonist naloxone. Endogenous opioid peptides concomitantly released by tissue stimulation also decreased norepinephrine release in a naloxone-sensitive manner. These results support the hypothesis that endogenous opioids can regulate excitability in the hippocampus by presynaptic modulation of norepinephrine release.

摘要

利用放射性配体置换分析法在豚鼠海马切片中检测到内源性去甲肾上腺素的释放。局灶性电刺激释放内源性去甲肾上腺素，并导致脑切片中β-肾上腺素能受体处特异性[³H]普萘洛尔结合的钙依赖性减少。μ-阿片受体激动剂PL017减少去甲肾上腺素释放，且PL017的抑制作用可被阿片受体拮抗剂纳洛酮阻断。组织刺激同时释放的内源性阿片肽也以纳洛酮敏感的方式减少去甲肾上腺素释放。这些结果支持这样一种假说，即内源性阿片类物质可通过对去甲肾上腺素释放的突触前调节来调节海马的兴奋性。