Can a Rat Tell You She Has a Headache? There’s More to Pain than Molecular Signaling
Kenneth E. McCarson, Ph.D.
Co-Director, Biobehavioral Measurement Core (BMC), Director, R.L. Smith IDDRC Rodent Behavior Facility , Kansas Intellectual and Developmental Disabilities Research Center (KIDDRC), Associate Professor, Department of Pharmacology, Toxicology and Therapeutics
Dr. McCarson has used rodent models of pain and behavioral measures in the study of the neurobiology of pain for well over two decades; as a postdoctoral Research Associate at Washington University these approaches were enhanced by acquiring the molecular tools used to expand my previous studies of the role of neurokinin receptors and tachykinin peptides, linking quantification of behavioral hyperalgesia (pain-related behaviors) with regulation of receptor gene expression in animal models of chronic inflammatory pain. As PI or co-Investigator on numerous university- and NIH-funded grants, I have expanded my studies into additional areas including cutaneous wound healing, GABAB receptor expression and function during pain, the molecular mechanisms underlying gender differences in chronic pain, hippocampal neurogenesis, hippocampal NK-1 receptor and BDNF expression and function, and the relationship between stress and chronic pain.
- Explain fundamental physiological mechanisms underlying pain sensation, including the spinal and supraspinal centers and systems that process pain and hyperalgesia.
- Describe plasticity of the neuronal systems and signals that contribute to sensitization to persistent pain.
- Explain sex differences in pain sensation, focusing on effects that estrogen can have to promote sensitization.
- Describe pain modeling in preclinical studies, focusing on rodent migraine modeling.
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