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摄取抑制剂拮抗对氯苯丙胺诱导的脑血清素耗竭的机制。

Mechanism by which uptake inhibitors antagonize p-chloroamphetamine-induced depletion of brain serotonin.

作者信息

Fuller R W

出版信息

Neurochem Res. 1980 Mar;5(3):241-5. doi: 10.1007/BF00964612.

DOI:10.1007/BF00964612
PMID:7374882
Abstract

The mechanism by which uptake inhibitors antagonize p-chloroamphetamine (PCA)-induced depletion of brain serotonin has been suggested to involve: (1) blockade of PCA uptake into the serotonin neuron by means of the membrane carrier, or (2) blockade of the efflux of released serotonin from the neuron, this efflux also requiring the membrane carrier. According to either mechanism, antagonism of serotonin depletion by PCA would provide a valid index of inhibition of the amine uptake system on serotonin neurons in vivo.

摘要

摄取抑制剂拮抗对氯苯丙胺（PCA）诱导的脑血清素耗竭的机制被认为涉及：（1）通过膜载体阻断PCA进入血清素神经元的摄取，或（2）阻断从神经元释放的血清素的流出，这种流出也需要膜载体。根据任何一种机制，PCA对血清素耗竭的拮抗作用都将提供体内血清素神经元上胺摄取系统抑制作用的有效指标。

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