Functional roles of endogenous D-serine in the chronic pain-induced plasticity of NMDAR-mediated synaptic transmission in the central amygdala of mice

被引:4
作者
Maekawa, Masao [1 ]
Wakamatsu, Shou [1 ]
Huse, Nozomi [1 ]
Konno, Ryuichi [2 ]
Hori, Yuuichi [1 ]
机构
[1] Dokkyo Med Univ, Sch Med, Dept Physiol & Biol Informat, Mibu, Tochigi 3210293, Japan
[2] Int Univ Hlth & Welf, Ctr Med Sci, Ohtawara, Tochigi 3248501, Japan
关键词
Serine racemase knockout mice; D-Serine; NMDAR mediated synaptic current; Amygdala; Chronic pain; PERIPHERAL-NERVE INJURY; RECEPTORS; NEURONS; RAT; PHOSPHORYLATION;
D O I
10.1016/j.neulet.2012.05.030
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The amygdala is implicated in chronic pain-induced emotional changes. Chronic pain induces plastic changes of the N-methyl-D-aspartate receptor (NMDAR) functions in the brain including the amygdala. D-Serine is synthesized endogenously by serine racemase and modulates NMDAR-mediated synaptic transmission as a coagonist of glycine binding site. To clarify the functional roles of endogenous D-serine in chronic pain-induced plasticity of NMDAR mediated synaptic transmission, we investigated the NMDAR-mediated excitatory synaptic current (EPSC) of neurons in the latero-capsular division of the central amygdala (CeLC) using brain slices from serine racemase knockout (SR-KO) mice with chronic pain induced by monoarthritis. The decay time of NMDAR-mediated EPSC was significantly elongated by monoarthritis in wild type (WT) mice, but not in SR-KO mice. The D-serine application-induced increase of NMDAR-mediated EPSC was significantly facilitated by monoarthritis in WT mice, but not in SR-KO mice. These results suggest that endogenous D-serine facilitates chronic pain-induced plastic changes of NMDAR mediated synaptic transmission in CeLC. (c) 2012 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:57 / 61
页数:5
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