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Visual stimuli-induced LTD of GABAergic synapses mediated by presynaptic NMDA receptors.由突触前NMDA受体介导的视觉刺激诱导的GABA能突触长时程抑制。
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腹侧被盖区及其他区域GABA能突触的长时程增强。

LTP of GABAergic synapses in the ventral tegmental area and beyond.

作者信息

Nugent Fereshteh S, Kauer Julie A

机构信息

Brown University, Department of Molecular Pharmacology, Physiology and Biotechnology, Providence, RI 02912, USA.

出版信息

J Physiol. 2008 Mar 15;586(6):1487-93. doi: 10.1113/jphysiol.2007.148098. Epub 2007 Dec 13.

DOI:10.1113/jphysiol.2007.148098
PMID:18079157
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2375707/
Abstract

One of the mechanisms by which the experience-dependent reorganization of neural circuitry can occur is through changes in synaptic strength. Almost every excitatory synapse in the mammalian brain exhibits LTP (long-term potentiation) or LTD (long-term depression), two cellular mechanisms of synaptic plasticity. However, LTP and LTD have been reported much more rarely at fast inhibitory GABA(A) receptor synapses. Our recent study suggests that in vivo morphine initiates a long-lasting alteration of GABAergic synapses in the ventral tegmental area (VTA) by blocking the mechanisms required for LTP of GABAergic synapses. Here we put this work into the context of other examples of synaptic plasticity at GABAergic synapses.

摘要

神经回路依赖经验的重组能够发生的一种机制是通过突触强度的改变。哺乳动物大脑中几乎每一个兴奋性突触都表现出长时程增强（LTP）或长时程抑制（LTD），这是突触可塑性的两种细胞机制。然而，在快速抑制性GABA(A)受体突触处，LTP和LTD的报道要少得多。我们最近的研究表明，体内吗啡通过阻断GABA能突触LTP所需的机制，引发腹侧被盖区（VTA）GABA能突触的长期改变。在此，我们将这项工作置于GABA能突触处其他突触可塑性例子的背景中。