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慢性疼痛的皮质前突触和后突触机制。

Presynaptic and postsynaptic cortical mechanisms of chronic pain.

机构信息

Department of Physiology, University of Toronto Centre for the Study of Pain, University of Toronto, Ontario, Canada.

出版信息

Mol Neurobiol. 2009 Dec;40(3):253-9. doi: 10.1007/s12035-009-8085-9. Epub 2009 Oct 11.

DOI:10.1007/s12035-009-8085-9
PMID:19821080
Abstract

Long-term potentiation (LTP) is a cellular model for learning and memory and believed to be critical for plastic changes in the brain. Depending on the central nervous system region, LTP has been proposed to contribute to many key physiological functions and pathological conditions, such as learning/memory, chronic pain, and drug addiction. While the induction of LTP in general requires activation of postsynaptic glutamate receptors, the expression of LTP can be mediated by postsynaptic mechanisms and/or presynaptic enhancement of glutamate release. In this review, we will evaluate recent progress made in the mechanisms of LTP in the anterior cingulate cortex (ACC) and explore its functional significance in synaptic changes after peripheral injury. Recent findings suggest that while ACC LTP in brain slice preparations is postsynaptically induced and expressed, injury triggered synaptic potentiation in the ACC contains both presynaptic enhancement of glutamate release and postsynaptic potentiation of AMPA receptor-mediated responses. Understanding presynaptic and postsynaptic mechanisms for ACC potentiation may help us to treat chronic pain in near future.

摘要

长时程增强(LTP)是学习和记忆的细胞模型,被认为对大脑的可塑性变化至关重要。根据中枢神经系统区域的不同,LTP 被认为有助于许多关键的生理功能和病理状况,如学习/记忆、慢性疼痛和药物成瘾。虽然一般来说,LTP 的诱导需要激活突触后谷氨酸受体,但 LTP 的表达可以通过突触后机制和/或突触前谷氨酸释放的增强来介导。在这篇综述中,我们将评估前扣带回皮层(ACC)中 LTP 机制的最新进展,并探讨其在外周损伤后突触变化中的功能意义。最近的发现表明,虽然脑片制备中的 ACC LTP 是突触后诱导和表达的,但损伤触发的 ACC 中的突触增强包含了谷氨酸释放的突触前增强和 AMPA 受体介导反应的突触后增强。了解 ACC 增强的突触前和突触后机制可能有助于我们在不久的将来治疗慢性疼痛。

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神经病理性疼痛大鼠模型中导水管周围灰质腺苷酸环化酶介导的谷氨酸能突触可塑性受损。
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