Synaptic and intrinsic plasticity in the ventral tegmental area after chronic cocaine.

Synaptic and intrinsic plasticity in the ventral tegmental area after chronic cocaine.
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DOI:
10.1016/j.conb.2018.08.013
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发表时间:
2019-02
影响因子:
5.7
通讯作者:
--
中科院分区:
医学2区
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--
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皮质醇暴露诱导腹侧被盖区(VTA)多巴胺神经元突触传递和内在特性的持续变化。尽管在理解可卡因诱导的可塑性方面取得了重大进展,但缺乏有效的可卡因成瘾治疗方法。慢性可卡因增强兴奋性并改变对多巴胺神经元的抑制性传递,诱导多巴胺神经元过度兴奋,并减少投射区的多巴胺释放。了解内在可塑性和突触可塑性如何相互作用以控制多巴胺神经元放电和多巴胺释放,可能有助于开发新的治疗方法。在这篇综述中,我们研究了最近的文献讨论可卡因诱导的可塑性在腹侧被盖区,并强调潜在的治疗干预。
Cocaine exposure induces persistent changes in synaptic transmission and intrinsic properties of ventral tegmental area (VTA) dopamine neurons. Despite significant progress in understanding cocaine-induced plasticity, an effective treatment of cocaine addiction is lacking. Chronic cocaine potentiates excitatory and alters inhibitory transmission to dopamine neurons, induces dopamine neuron hyperexcitability, and reduces dopamine release in projection areas. Understanding how intrinsic and synaptic plasticity interact to control dopamine neuron firing and dopamine release could prove useful in the development of new therapeutics. In this review, we examine recent literature discussing cocaine-induced plasticity in the VTA and highlight potential therapeutic interventions.
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