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

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...

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Bibliographic Details
Published in:Neuroscience letters 2001-01, Vol.297 (1), p.25-28
Main Authors: Wake, Kohji, Yamazaki, Hajime, Hanzawa, Shinji, Konno, Ryuichi, Sakio, Hideaki, Niwa, Akira, Hori, Yuuichi
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
d-Amino-acid oxidase
D-Amino-Acid Oxidase - deficiency
d-Serine
Excitatory Postsynaptic Potentials - genetics
Formalin test
Fundamental and applied biological sciences. Psychology
Mice
Mice, Mutant Strains
N-Methyl- d-aspartate receptors
Pain Measurement - methods
Posterior Horn Cells - physiology
Receptors, N-Methyl-D-Aspartate - genetics
Somesthesis and somesthetic pathways (proprioception, exteroception, nociception)
interoception
electrolocation. Sensory receptors
Synaptic Transmission - genetics
Synaptic Transmission - physiology
Tonic pain
Vertebrates: nervous system and sense organs
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Summary: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.
ISSN:0304-3940
1872-7972
DOI:10.1016/S0304-3940(00)01658-X