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长期使用苯环利定会增加前额叶皮质和伏隔核神经元的树突棘密度。

Chronic phencyclidine treatment increases dendritic spine density in prefrontal cortex and nucleus accumbens neurons.

作者信息

Flores Cecilia, Wen Xianglan, Labelle-Dumais Cassandre, Kolb Bryan

机构信息

Departement of Psychiatry and of Neurology and Neurosurgery, McGill University, Douglas Hospital Research Centre, 6875 LaSalle Boulevard, Quebec, Canada, H4H 1R3.

出版信息

Synapse. 2007 Dec;61(12):978-84. doi: 10.1002/syn.20452.

DOI:10.1002/syn.20452
PMID:17879264
Abstract

We examined whether repeated exposure to the noncompetitive NMDA receptor antagonist phencyclidine (PCP) produces enduring changes in dendritic structure in a manner similar to the stimulants cocaine and amphetamine. Adult rats were treated with i.p. injections of PCP (5 mg/kg) or saline, twice a day, for 5 consecutive days, for a total of 4 weeks. One month after the last injection, their brains were removed and processed for Golgi-Cox staining. Prior exposure to PCP increased dendritic spine density in the mPFC and NAcc core, but not in the parietal cortex. These findings, which are similar to those observed after chronic treatment with cocaine and amphetamine, raise the possibility that, despite differences in their mechanisms of action, PCP and stimulant drugs may induce some of their enduring effects via common processes.

摘要

我们研究了反复接触非竞争性N-甲基-D-天冬氨酸(NMDA)受体拮抗剂苯环利定(PCP)是否会以类似于兴奋剂可卡因和苯丙胺的方式对树突结构产生持久变化。成年大鼠每天腹腔注射PCP(5mg/kg)或生理盐水,连续5天,每天2次,共4周。最后一次注射后1个月,取出它们的大脑并进行高尔基-考克斯染色处理。先前接触PCP可增加内侧前额叶皮质(mPFC)和伏隔核核心区的树突棘密度,但顶叶皮质未增加。这些发现与可卡因和苯丙胺慢性治疗后观察到的结果相似,这增加了一种可能性,即尽管PCP和兴奋剂药物的作用机制不同,但它们可能通过共同的过程诱导一些持久效应。

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