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Gary Strichartz, Ph.D.

Professor of Anaesthesia (Pharmacology)

Brigham and Women's Hospital
Anaesthesia
75 Francis St
Boston, MA 02115
Telephone: 617-732-7802
Fax: 617-730-2801
Email: gstrichz@zeus.bwh.harvard.edu
Predocs: 0 Postdocs: 4 Completed PhD's: 6

Gary Strichartz

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.

 

References:

  • Amir R, Argoff CE, Bennett GJ, Cummins TR, Durieux ME, Gerner P, Gold MS, Porreca F, Strichartz GR. The role of sodium channels in chronic inflammatory and neuropathic pain. J Pain 2006, 7 (Supplement 3): S1-S29.

  • Balonov K, Khodorova A,  Strichartz, GR. Tactile allodynia initiated by local   subcutaneous   endothelin-1 is prolonged by activation of TRPV-1 receptors. Exp Biol Med 2006, 231:1165-70.

  • Zhuang Z-Y, Wen Y-R, Zhang D-R, Borsello T, Bonny C, Strichartz GR, Decosterd I, Ji R-R. A peptide JNK inhibitor blocks mechanical allodynia after spinal nerve ligation: respective roles of JNK activation in primary sensory neurons and spinal astrocytes for neuropathic pain development and maintenance. J Neurosci 2006, 26: 3551-3560.

  • Yanagidate F and Strichartz, GR. Bupivacaine inhibits activation of   neuronal spinal extracellular receptor activated kinase through selective effects on ionotropic receptors. Anesthesiology  2006, 104: 805-814.

  • Mujenda FH, Duarte AM, Reilly EK, Strichartz GR. Cutaneous endothelin-A   receptors elevate post-incisional pain.  Pain 2007, (in press; doi.10.1016/j.pain.2007.03.021.)