Kenneth McCarson Ph.D.
Director, SensoriMotor Rodent Behavior FacilityKansas Intellectual and Developmental Disabilities Research Center
University of Kansas - Lawrence
Kansas University Medical Center
3901 Rainbow Blvd
Kansas City, KS 66160
913-588-7519 (tel)
[email protected]
http://www2.kumc.edu/mrrc/rbfsm/index.html
Biography/Curriculum Vitae:
Research Interests:
Our research program examines the role that altered gene expression of various neurotransmitters and their receptors plays in the regulation of sensory function, and particularly focuses of the role of neurokinin (NK-1) receptors in chronic inflammatory pain. The plasticity of neurokinin receptor gene expression in the spinal cord provides a molecular marker for the activation of sensory systems by long-lasting noxious stimuli that may contribute to central sensitization and increased responsiveness to subsequent stimuli (hyperalgesia and allodynia). Several studies have addressed the pattern of NK-1 receptor gene expression and the regulation of NK-1 gene expression by other products of persistent pain in the rat; others have addressed the role of the NK-1 receptor in sensory systems and their relationship to areas of the brain involved in the regulation of affect (or mood) and the similarity of these phenomena to those produced by acute and chronic immobilization stress. Our research also investigates gender-related differences in the degree of activation of NK-1 and BDNF gene expression by inflammation in peripheral sites of inflammation, in tissues associated with pain processing, as well as higher brain centers associated with emotions and mood. The demonstration that the degree of pain-evoked BDNF gene expression varies directly with estrogen status provides compelling evidence for estrogen sensitivity of the mechanisms underlying aspects of chronic pain and depression. Studies also address changes in G-protein coupled intracellular signaling that occur during long-term nociceptive activation of neurokinin receptors in sensory systems. Recent results have demonstrated time-dependent changes in the affinity and coupling of spinal NK-1 receptors, suggesting that their cellular function is subject to regulation by the neuronal activation produced by inflammatory pain. Other active areas of investigation in the laboratory include the role of neurokinin-expressing sensory nerves in cutaneous wound healing and the characterization of vanilloid receptor integration of thermal and acidic stimuli in amphibian sensory systems. This research has important consequences related to our understanding of pain and inflammation by clarifying the involvement of neurokinin receptor function in the sensitization of the central nervous system by long-term pain, and may identify novel targets or therapies for the control of the sensitizing effects of chronic pain resulting from neurokinin receptor plasticity. 913-588-7519 [email protected]
Narrative of Current Research Efforts:
Major Honors and Awards:
Representative Publications:
Created 1/5/2006 by Evette Mezger
Last modified 3/30/2006 by Evette Mezger
