Suppr超能文献

豚鼠啃咬癖与中枢多巴胺能机制的关系(作者译)

[Relationship between gnawing compulsion and central dopaminergic mechanism in guinea pigs (author's transl)].

作者信息

Uemura H

出版信息

Nihon Yakurigaku Zasshi. 1979 Jan;75(1):61-72. doi: 10.1254/fpj.75.61.

Abstract

It has been reported that an increased in dopaminergic activity in the striatum can induce gnawing compulsion, a stereotyped behavior. Apomorphine, amphetamine and L-DOPA also produce such effects, particularly in the rat. However, it has been reported that the gnawing compulsion in the guinea pig cannot be induced with L-DOPA and is not related to the levels of catecholamine in the brain. It is of essential importance in this kind of research to clarify whether or not a dopaminergic mechanism is equally involved in gnawing compulsion of the rodent in general. The present study dealt with the mechanism of gnawing compulsion with L-DOPA administration to guinea pigs. Gnawing compulsion was amplified by crystal pick-up and amplifiers and was continuously recorded by an inkwriting-oscilloscope. The recorded data were scored for quantitative and objective analysis. Certainly, L-DOPA alone did not induce continuous gnawing, but the gnawing was obviously induced by pretreatment with benserazide, a peripheral decarboxylase inhibitor. The induced gnawing complusion was inhibited by pimozide and haloperidol which are both dopamine receptor blockers. When catecholamine synthesis was inhibited pretreatment with alpha-methyl-p-tyrosine, the amphetamine induced gnawing compulsion alone was markedly inhibited, but the apomorphine or L-DOPA induced gnawing compulsion following the pretreatment with benserazide was not inhibited. Therefore, it was deduced that gnawing compulsion was induced with amphetamine directly by dopamine release, with apomorphine by its direct stimulation of the dopamine receptor, and with L-DOPA by its action on the dopamine receptor, after having been converted to dopamine. Based on these results, it was concluded that the dopaminergic mechanism is closely involved in gnawing compulsion seen in the guinea pig as well as in the rat.

摘要

据报道,纹状体中多巴胺能活性增加可诱发啃咬强迫行为,这是一种刻板行为。阿扑吗啡、苯丙胺和左旋多巴也会产生这种效应,尤其是在大鼠中。然而,据报道,左旋多巴不能诱发豚鼠的啃咬强迫行为,且该行为与大脑中的儿茶酚胺水平无关。在这类研究中,明确多巴胺能机制是否同样参与一般啮齿动物的啃咬强迫行为至关重要。本研究探讨了给豚鼠注射左旋多巴后啃咬强迫行为的机制。啃咬强迫行为通过拾音器和放大器放大,并由墨水书写示波器连续记录。对记录的数据进行评分以进行定量和客观分析。当然,单独使用左旋多巴不会诱发持续的啃咬行为,但外周脱羧酶抑制剂苄丝肼预处理后明显诱发了啃咬行为。诱导的啃咬强迫行为被多巴胺受体阻滞剂匹莫齐特和氟哌啶醇抑制。当用α-甲基-对-酪氨酸预处理抑制儿茶酚胺合成时,单独的苯丙胺诱导的啃咬强迫行为明显受到抑制,但苄丝肼预处理后阿扑吗啡或左旋多巴诱导的啃咬强迫行为未受到抑制。因此,推断苯丙胺通过释放多巴胺直接诱发啃咬强迫行为,阿扑吗啡通过直接刺激多巴胺受体诱发,左旋多巴通过转化为多巴胺后作用于多巴胺受体诱发。基于这些结果,得出结论:多巴胺能机制与豚鼠和大鼠中出现的啃咬强迫行为密切相关。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验