| First Author | Wake K | Year | 2001 |
| Journal | Neurosci Lett | Volume | 297 |
| Issue | 1 | Pages | 25-8 |
| PubMed ID | 11114476 | Mgi Jnum | J:107977 |
| Mgi Id | MGI:3622612 | Doi | 10.1016/s0304-3940(00)01658-x |
| Citation | Wake K, et al. (2001) Exaggerated responses to chronic nociceptive stimuli and enhancement of N-methyl-D-aspartate receptor-mediated synaptic transmission in mutant mice lacking D-amino-acid oxidase. Neurosci Lett 297(1):25-8 |
| abstractText | Formalin-induced nociceptive behaviors and N-methyl-D-aspartate (NMDA) subtype glutamate receptor-mediated excitatory synaptic transmission were analyzed in mutant mice lacking D-amino-acid oxidase, which catalyzes the oxidative deamination of D-amino acids. The second phase of the formalin-induced licking response, a part of which is known to be mediated by NMDA receptors in the spinal cord, was significantly augmented in mutant mice. NMDA receptor-mediated excitatory postsynaptic currents recorded from spinal cord dorsal horn neurons by tight-seal whole-cell methods were significantly potentiated in mutant mice. The present observations provide another line of evidence that D-serine functions as an endogenous coagonist at the glycine site of NMDA receptors, and raise the possibility that D-amino-acid oxidase exerts a neuromodulatory function by controlling the concentration of D-serine in the central nervous system. |
