Chronic neuropathic pain results from nerve injury. It is a source of unrelenting agony for millions of Americans since there are no effective pharmacotherapies available. In light of the significant increases in the incidence of diabetes, road traffic accidents, tuberculosis, cancer and major surgical interventions, which lead to neuropathic pain states, it is likely that this problem will continue to present challenges to treatment. A major complain of neuropathic pain patients is a constant burning together with intermittent pain often described as shooting, electric shock-like, the feeling of walking on broken glass, or the sensation of bugs crawling under skin. The mechanism underlying this spontaneous neuropathic pain (SNP) is thought to include abnormal spontaneous activity of the peripheral pain sensing receptors, nociceptors. Few explanations have been advanced to explain why and how nociceptors fire spontaneously in these neuropathic pain states.
New research in this laboratory focuses on identifying the role of TrpV1, a heat activated receptor, in SNP and will evaluate the overall hypothesis that TrpV1 mediated abnormal firing of nociceptors leads to SNP-like behaviors in an animal model of nerve injury. Upon completion of this stuffy, we expect to have clarified the precise function and significance of TrpV1 in the physiological and behavioral mechanisms of nerve-injury related pain. The results of this research will provide the scientific basis for the development of new, effective and specific pharmacotherapeutics.