Gary Strichartz, Ph.D.
Professor of Anaesthesia (Pharmacology)
Department of Anaesthesia, MRB 611
75 Francis Street
Boston, MA 2115
My laboratory is studying the cellular mechanisms that are essential for the induction and, especially, the persistence of pain, triggered by tissue injury or caused by disease. Using a multi-disciplinary approach, we quantify animals’ pain behavior, conduct electrophysiological experiments on isolated skin and nerve, measure other cellular and biochemical responses, such as intracellular [Ca+2] and cAMP, to determine intracellular pathways, and apply chemical agents to the periphery and spinal cord in efforts to prevent or reverse persisting pain. We also investigate the sites and micro-anatomical changes of receptors and signals, using immunocytochemistry.
Our work is particularly focussed now on the activation of MAPkinases in skin and peripheral nerve, as well as spinal cord, after injury or surgery, and also on the role of receptors for the endogenous peptide endothelin-1 (ET-1), which is secreted by metastasizing cancer cells and which also causes pain when delivered to normal skin and nerve. ET-1 selectively activates nociceptors in vivo, causes release of intracellular Ca+2 in isolated neurons in vitro, and effects ion channels via GPCR-coupled reactions. ET-1 also induces the release of β-endorphin from cultured skin cells, and effects a cutaneous, opioid-receptor linked analgesia. We believe that these dual, competing effects, on cutaneous nerves and on keratinocytes, temper responses to peripheral insults in healthy subjects, but that during some diseases and after injury and inflammation this balance is tipped in favor of the pro-algesic reactions that result in pain.
For a complete listing of publications click here.
Last Update: 10/30/2013