Glycine inhibitory dysfunction provides a useful experimental model for studying the
mechanism of dynamic mechanical allodynia, a widespread and intractable symptom of
neuropathic pain. In this model, allodynia expression relies on N-methyl-d-aspartate
receptors (NMDARs), and it has been shown that astrocytes can regulate their activation
through the release of the NMDAR coagonist d-serine. Recent studies also suggest that
astrocytes potentially contribute to neuropathic pain. However, the involvement of astrocytes …