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5-羟色胺1A受体与认知记忆。氮能系统对其行为效应的可能调节作用。

The 5-HT1A receptor and recognition memory. Possible modulation of its behavioral effects by the nitrergic system.

作者信息

Pitsikas Nikolaos, Tsitsirigou Stavroula, Zisopoulou Styliani, Sakellaridis Nikolaos

机构信息

Department of Pharmacology, School of Medicine, University of Thessaly, 22 Papakiriazi Str., 412-22 Larissa, Greece.

出版信息

Behav Brain Res. 2005 Apr 30;159(2):287-93. doi: 10.1016/j.bbr.2004.11.007. Epub 2004 Dec 13.

DOI:10.1016/j.bbr.2004.11.007
PMID:15817191
Abstract

Functional activation of the 5-HT1A receptor inhibits cognition, although discrepant findings have also been reported. The present study was designed to investigate the role of the 5-HT1A receptor on recognition memory in the rat. For this purpose, the effects induced by the 5-HT1A agonist R-(+)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT) and the 5-HT1A antagonist WAY 100635 on memory were evaluated by using the object recognition task. In addition, the possible involvement of the nitrergic system on 5-HT1A receptor's effects was also assessed by using the same behavioral procedure. In the first dose-response study, post-training administration of 8-OH-DPAT (0.1 and 0.3 mg/kg, subcutaneously (s.c.)) dose-dependently impaired animals' performance in this test. WAY 100635 (0.3 and 1 mg/kg, intraperitoneally (i.p.)) successfully antagonized these 8-OH-DPAT-induced performance deficits. The NO donor molsidomine (2 and 4 mg/kg, i.p.) counteracted cognition deficits produced by the highest dose of 8-OH-DPAT (0.3 mg/kg). Our findings indicate (a) that the 5-HT1A receptor is involved in recognition memory, and (b) that a NO component modulates the effects of the 5-HT1A receptor on learning and memory.

摘要

5-HT1A 受体的功能激活会抑制认知,尽管也有不一致的研究结果报道。本研究旨在探讨 5-HT1A 受体在大鼠识别记忆中的作用。为此,通过物体识别任务评估了 5-HT1A 激动剂 R-(+)-8-羟基-2-(二正丙基氨基)四氢萘溴化物(8-OH-DPAT)和 5-HT1A 拮抗剂 WAY 100635 对记忆的影响。此外,还通过相同的行为学程序评估了硝化系统对 5-HT1A 受体作用的可能参与情况。在第一项剂量反应研究中,训练后皮下注射 8-OH-DPAT(0.1 和 0.3 mg/kg)剂量依赖性地损害了动物在该测试中的表现。腹腔注射 WAY 100635(0.3 和 1 mg/kg)成功拮抗了这些由 8-OH-DPAT 诱导的表现缺陷。NO 供体吗多明(2 和 4 mg/kg,腹腔注射)抵消了最高剂量 8-OH-DPAT(0.3 mg/kg)产生的认知缺陷。我们的研究结果表明:(a)5-HT1A 受体参与识别记忆;(b)NO 成分调节 5-HT1A 受体对学习和记忆的作用。

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