Intracellular 5-HT 2C-receptor dephosphorylation: a new target for treating drug addiction.
Intracellular 5-HT 2C-receptor dephosphorylation: a new target for treating drug addiction.
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细胞内 5-HT 2C 受体去磷酸化：治疗药物成瘾的新靶点。
DOI：
10.1016/j.tips.2006.07.003
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Carey,RobertJ
中科院分区：
文献类型：
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作者：
Muller,ChristianP;Carey,RobertJ
5-羟色胺（5-HT）2C受体作为治疗药物成瘾的靶点受到了广泛关注。然而，5-HT 2C受体激动剂也诱导副作用。本文就5-HT 2C受体参与动物药物成瘾行为的研究进展作一综述。最近显示，使用蛋白肽达特-3L 4 F可以在细胞内诱导5-HT 2C-受体激动剂作用，所述蛋白肽防止由10号染色体上缺失的磷酸酶和张力蛋白同源物诱导的5-HT 2C-受体去磷酸化。最有希望的发现是，达特-3L 4 F可以通过减少中脑边缘多巴胺传递而选择性地降低成瘾药物的效力，而不会引起5-HT 2C受体激动剂治疗的副作用，从而突出了其作为治疗人类药物成瘾的策略的潜在用途。
The 5-hydroxytryptamine (5-HT)2Creceptor has received considerable attention as a target for treating drug addiction. 5-HT2C-receptor agonism, however, also induces side-effects. In this article, we review recent findings regarding the involvement of 5-HT2Creceptors in behaviours related to drug addiction in animals. It was recently shown that 5-HT2C-receptor agonist effects can be induced intracellularly using the protein peptide Tat–3L4F, which prevents 5-HT2C-receptor dephosphorylation induced by phosphatase and tensin homologue deleted on chromosome 10. The most promising finding is that Tat–3L4F can selectively reduce the potency of addictive drugs by reducing mesolimbic dopamine transmission without eliciting the side-effects of 5-HT2C-receptor agonist treatment, thus highlighting its potential use as a strategy to treat drug addiction in humans.