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基于中脑缝际电极植入的自我刺激的神经化学基础。

On the neurochemical basis of self-stimulation with midbrain raphe electrode placements.

作者信息

Deakin J F

出版信息

Pharmacol Biochem Behav. 1980 Oct;13(4):525-30. doi: 10.1016/0091-3057(80)90275-0.

Abstract

Bar-pressing for electrical stimulation of the median raphe nucleus in rats was not attenuated by 5HT receptor blockade with metergoline or cyproheptadine, by 5HT depletion induced with parachloroamphetamine or by prior destruction of ascending 5HT pathways with intracerebral microinjections of 5,7-dihydroxytryptamine. Furthermore, in a shuttle box paradigm in which rats could both initiate and terminate stimulation, parachlorophenylalanine did not antagonize initiation of stimulation. It is concluded that the rewarding effects of raphe stimulation are not mediated by serotonergic mechanisms. In contrast to these results, alpha-methyl-paratyrosine induced catecholamine depletion exerted an inhibitory effect on initiation behaviour without impairing termination of stimulation. It is concluded that the rewarding component of raphe stimulation is mediated by catecholamines. Termination of (escape from) stimulation was not materially affected by catecholamine or 5HT depletion suggesting the aversive component of raphe stimulation may not be mediated by these monoamines.

摘要

用美替拉酮或赛庚啶进行5-羟色胺(5HT)受体阻断、用对氯苯丙胺诱导5HT耗竭,或事先通过脑内微量注射5,7-二羟色胺破坏5HT上行通路,均不会减弱大鼠为获得中缝核电刺激而进行的压杆行为。此外,在一个大鼠既能启动又能终止刺激的穿梭箱范式中,对氯苯丙氨酸不会拮抗刺激的启动。得出的结论是,中缝核刺激的奖赏效应不是由5-羟色胺能机制介导的。与这些结果相反,α-甲基-对酪氨酸诱导的儿茶酚胺耗竭对启动行为产生了抑制作用,但不影响刺激的终止。得出的结论是,中缝核刺激的奖赏成分是由儿茶酚胺介导的。刺激的终止(逃避)不受儿茶酚胺或5HT耗竭的实质性影响,这表明中缝核刺激的厌恶成分可能不是由这些单胺介导的。

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