New and emerging pharmacological targets for neuropathic pain.
Increasing knowledge of the molecular consequences of nerve injury and the availability of genome databases has greatly increased the range of potential targets for the pharmacological management of neuropathic pain. Controlling neuronal sensitization and the associated alterations in gene expression, protein modification, and neuronal excitability is the key to managing neuropathic pain. Control of neuronal sensitization can occur through inhibition of nerve injury-associated production of cytokines, activation of glial cells, modulation of potassium channel subtypes, mitogen-activated protein kinases, the ubiquitin-proteasome system, or the protection and amplification of spinal cord dorsal horn inhibitory systems. These new and already established targets promise unparalleled opportunities for the prevention, management, and resolution of persistent pain states following nerve injury.
Manning
Donald C
DC
Clinical Research and Development, Celgene Corporation, Seven Powder Horn Drive, Warren, NJ 07059, USA. dmanning@celgene.com
D016207:Cytokines / Q000187:drug effects / Q000502:physiology; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000187:drug effects / Q000502:physiology; D009437:Neuralgia / Q000188:drug therapy* / Q000503:physiopathology; D009457:Neuroglia / Q000187:drug effects / Q000502:physiology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology; D043743:Ubiquitin-Protein Ligase Complexes / Q000187:drug effects / Q000502:physiology
D016207:Cytokines; D015221:Potassium Channels; D043743:Ubiquitin-Protein Ligase Complexes; D020928:Mitogen-Activated Protein Kinases