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多巴胺能和5-羟色胺能系统损伤对大鼠阿扑吗啡诱导的体温过低的影响。

The effect of lesions of dopaminergic and serotonergic systems on apomorphine-induced hypothermia in the rat.

作者信息

Przewlocki R

出版信息

Pol J Pharmacol Pharm. 1977 May-Jun;29(3):263-70.

PMID:887502
Abstract

Bilateral lesion of caudate nucleus or substantia nigra as well as brain transsection between telencephalon and diencephalon potentiates the body temperature fall produced by apomorphine (5 mg/kg). A lesion of nucleus accumbens septi did not prevent the hypothermia, but slightly shortened its duration. Electrolytical and chemical (with 5,6-dihydroxytryptamine) lesions of both dorsal and medial raphe nuclei alleviated the hypothermia produced by apomorphine. The lesion of medial raphe nucleus did not affect, while the lesion of dorsal raphe nucleus prevented the hypothermia induced by apomorphine or piribedil (25 mg/kg). The results show that dopaminergic neurons of telencephalon are not involved in the mechanism of induction of apomorphine hypothermia, while the neurons of dorsal raphe nucleus participate in it.

摘要

尾状核或黑质的双侧损伤以及端脑与间脑之间的脑横断会增强阿扑吗啡(5毫克/千克)引起的体温下降。伏隔核损伤并不能预防体温过低,但会略微缩短其持续时间。背侧和中缝核的电解损伤和化学损伤(用5,6 - 二羟基色胺)可减轻阿扑吗啡引起的体温过低。中缝核损伤不影响,而背侧中缝核损伤可预防阿扑吗啡或匹莫齐尔(25毫克/千克)诱导的体温过低。结果表明,端脑的多巴胺能神经元不参与阿扑吗啡性体温过低的诱导机制,而背侧中缝核的神经元参与其中。

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