Suppression of neuropathic pain hypersensitivity by TRPM8 is mediated by mGluR group II and III receptors acting differentially on distinct nociceptor inputs to spinal cord
Sue Fleetwood-Walker
BackgroundChronic pain following nerve injury (neuropathic pain), is notoriously difficult to treat, with current analgesics showing limited efficacy and adverse or dangerous side effects. One new candidate analgesic target is the TRPM8 ion channel, identified as the peripheral detector for innocuous cool sensation and reported to attenuate spinal cord pain processing by processes involving inhibitory metabotropic glutamate (mGlu) receptors.MethodsHighly selective Group II/III mGluR antagonists