将α-芋螺毒素MII和AuIB微量注射到大鼠蓝斑中对尼古丁诱导的海马去甲肾上腺素释放的抑制作用

Inhibition of nicotine-induced hippocampal norepinephrine release in rats by alpha-conotoxins MII and AuIB microinjected into the locus coeruleus.

作者信息

Fu Y, Matta S G, McIntosh J M, Sharp B M

机构信息

Department of Pharmacology, University of Tennessee-Memphis, 38163, USA.

出版信息

Neurosci Lett. 1999 May 7;266(2):113-6. doi: 10.1016/s0304-3940(99)00293-1.

DOI:10.1016/s0304-3940(99)00293-1

PMID:10353340

Abstract

Hippocampal norepinephrine (NE) is secreted by neurons projecting from the locus coeruleus (LC) to the hippocampus; LC nicotinic receptors (NAchRs) are involved in the effects of systemic nicotine on this pathway. To clarify the NAchR subtypes, NAchR antagonists, termed alpha-conotoxins, were microinjected into the LC before nicotine; MII and AuIB were used to assess the potential involvement of alpha3beta2 and alpha3beta4 subunit-containing NAchRs, respectively. Nicotine dose-dependently stimulated hippocampal NE release (P < 0.01). MII (>0.25 pmol) reduced the NE response to nicotine (67% decrease; P < 0.05), as did AuIB (44% reduction by 25 pmol; P < 0.05). Administered together, however, MII and AuIB were no more effective than MII. Thus, MII and AuIB are capable of interacting with NAchR subtypes other than those previously defined as alpha3beta2 and alpha3beta4, respectively. NAchRs containing both beta2 and beta4-subunits may be involved.

摘要

海马体中的去甲肾上腺素（NE）由从蓝斑（LC）投射到海马体的神经元分泌；LC烟碱型受体（NAchRs）参与全身尼古丁对该通路的作用。为了阐明NAchR亚型，在注射尼古丁之前，将称为α-芋螺毒素的NAchR拮抗剂微量注射到LC中；分别使用MII和AuIB来评估含α3β2和α3β4亚基的NAchRs的潜在参与情况。尼古丁剂量依赖性地刺激海马体NE释放（P < 0.01）。MII（>0.25 pmol）降低了对尼古丁的NE反应（降低67%；P < 0.05），AuIB（25 pmol时降低44%；P < 0.05）也是如此。然而，MII和AuIB一起给药时并不比单独使用MII更有效。因此，MII和AuIB能够与先前分别定义为α3β2和α3β4之外的NAchR亚型相互作用。可能涉及同时含有β2和β4亚基的NAchRs。