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司来吉兰和β-苯乙胺对Wistar大鼠的行为和神经化学影响。

Behavioral and neurochemical effects of deprenyl and beta-phenylethylamine in Wistar rats.

作者信息

Greenshaw A J, Juorio A V, Boulton A A

出版信息

Brain Res Bull. 1985 Aug;15(2):183-9. doi: 10.1016/0361-9230(85)90134-0.

Abstract

The effects of 1-deprenyl (1-16 mg kg-1, 3.5 hr) on brain levels of endogenous beta-phenylethylamine were assessed in animals under three conditions: (1) experience of lateral hypothalamic self-stimulation; (2) electrode implantation but no self-stimulation experience; (3) no surgical intervention. The increase in striatal levels of beta-phenylethylamine with 1-deprenyl treatment was attenuated in the self-stimulation condition relative to conditions (2) and (3). This differential effect of 1-deprenyl was not observed at the level of the hypothalamus. Administration of 1-deprenyl did not affect self-stimulation behavior. Equivalent analysis of beta-phenylethylamine levels was carried out using animals injected with beta-phenylethylamine (0.5-4 mg kg-1, 0.5 hr 1P and 1-deprenyl (4 mg kg-1, 3.5 hr sc). Injected beta-phenylethylamine with deprenyl pretreatment increased self-stimulation rates; concomitant striatal levels of approximately 190 ng g-1 of beta-phenylethylamine were observed and were associated with increased brainstem 5-HIAA but no change in striatal HVA, indicating possible involvement of 5-HT in this response to beta-phenylethylamine. It is proposed that experience of electrical hypothalamic stimulation may alter endogenous striatal beta-phenylethylamine metabolism, possibly via an alteration of mechanisms governing synthesis and/or catabolism.

摘要

在三种条件下评估了1-司来吉兰(1 - 16毫克/千克,3.5小时)对动物脑内源性β-苯乙胺水平的影响:(1)下丘脑外侧自我刺激经历;(2)植入电极但无自我刺激经历;(3)无手术干预。与条件(2)和(3)相比,在自我刺激条件下,1-司来吉兰处理使纹状体β-苯乙胺水平的升高减弱。在下丘脑水平未观察到1-司来吉兰的这种差异效应。给予1-司来吉兰不影响自我刺激行为。使用注射了β-苯乙胺(0.5 - 4毫克/千克,0.5小时腹腔注射)和1-司来吉兰(4毫克/千克,3.5小时皮下注射)的动物进行了β-苯乙胺水平的等效分析。预先用司来吉兰处理后注射β-苯乙胺可提高自我刺激率;观察到纹状体β-苯乙胺水平约为190纳克/克,同时脑干5-羟吲哚乙酸增加,但纹状体高香草酸无变化,表明5-羟色胺可能参与了对β-苯乙胺的这种反应。有人提出,下丘脑电刺激经历可能改变内源性纹状体β-苯乙胺代谢,可能是通过改变合成和/或分解代谢的调控机制。

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