| First Author | Maekawa M | Year | 2012 |
| Journal | Neurosci Lett | Volume | 520 |
| Issue | 1 | Pages | 57-61 |
| PubMed ID | 22609571 | Mgi Jnum | J:188813 |
| Mgi Id | MGI:5442258 | Doi | 10.1016/j.neulet.2012.05.030 |
| Citation | Maekawa M, et al. (2012) Functional roles of endogenous D-serine in the chronic pain-induced plasticity of NMDAR-mediated synaptic transmission in the central amygdala of mice. Neurosci Lett 520(1):57-61 |
| abstractText | 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. |
