Journal
SCIENCE
Volume 300, Issue 5628, Pages 2094-2097Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1083970
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In the mammalian CNS, N-methyl-D-aspartate ( NMDA) receptors serve prominent roles in many physiological and pathophysiological processes including pain transmission. For full activation, NMDA receptors require the binding of glycine. It is not known whether the brain uses changes in extracellular glycine to modulate synaptic NMDA responses. Here, we show that synaptically released glycine facilitates NMDA receptor currents in the superficial dorsal horn, an area critically involved in pain processing. During high presynaptic activity, glycine released from inhibitory interneurons escapes the synaptic cleft and reaches nearby NMDA receptors by so-called spillover. In vivo, this process may contribute to the development of inflammatory hyperalgesia.
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