Musculoskeletal Pain Lab
Chronic pain especially that associated with musculoskeletal tissue is a significant clinical problem that affects a large percent of the population and has a major economic impact on the health care system. Despite the clinical significance mechanisms underlying the development and maintenance of persistent pain conditions arising from deep tissue, and cellular mechanisms involved in the transition from acute to chronic pain conditions are not clearly understood. The objectives of my research have been the development of reliable animal behavioral models that assess acute and chronic changes in deep tissue sensitivities, and to elucidate cellular and molecular mechanisms of acute and chronic muscle and joint pain using the craniofacial deep tissue as a model system.
We are currently working on two major projects funded by NIH: (1) Investigate the role of peripheral receptor systems in overt muscle nociception and in mechanical hyperalgesia. Specifically, we are investigating potential mechanisms that underlie the development of mechanical hyperalgesia with a particular emphasis on functional coupling between peripherally localized NMDA and metabotropic glutamate receptors and TRPV1 and TRPA1 channels in the context of craniofacial muscle pain,
(2) Study the factors that contribute to sex-differences in molecular, cellular, and function properties in peripheral antinociceptove systems that include opioid receptors, cannabinoid receptors and potassium channels. We primarily focus on examining novel mechanisms by which sex differences in antinociceptive systems are expressed in the context of inflammatory muscle pain conditions.
(3) In addition, we have an ongoing project that explores whether nitric oxide (NO) in the trigeminal sensory nuclear complex (TSNC) that is closely regulated by both neurons and non-neuronal cells play as a critical mediator in the pathogenesis of both acute and chronic orofacial muscle pain conditions. Specific hypotheses of this proposal are that acute and chronic masseter inflammation differentially regulate nitric oxide synthase (NOS) from neuronal and non-neuronal cells (i.e., nNOS, iNOS, and eNOS), the regulation of NO level by iNOS is critical in the development of chronic muscle hypealgesia, and that the blockade of iNOS-NO-neuronal sGC pathway results in attenuation of orofacial muscle pain and hyperalgesia.
Pain, Muscle, Inflammation, Sensory Neurons, Peripheral Sensitization, Glutamate Receptors, TRP Channels, Opioid Receptors, Cannabinoid Receptors, Sex Hormones, Cytokines, Nitric Oxide