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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
Lab Website: The Strichartz Lab

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:

  • Yanagidate F and Strichartz, GR. (2006) Bupivacaine inhibits activation of   neuronal spinal extracellular receptor activated kinase through selective effects on ionotropic receptors. Anesthesiology  104: 805-814.
  • Mujenda FH, Duarte AM, Reilly EK, Strichartz GR. (2007) Cutaneous endothelin-A   receptors elevate post-incisional pain.  Pain 2007, (in press; doi.10.1016/j.pain.2007.03.021.)
  • Sugimoto K, Kissin I, Strichartz GR.  (2008) High concentrations of resiniferatoxin inhibit ioni channel function in clonal neuroendocrine cells.  Anesth. Analg. 107:318-324.
  • Strichartz GR.  (2008) Novel ideas of local anaesthetic actions on various ion channels to ameliorate post-operative pain.  Br. J. Anaesth. 101(1):45-7.  doi: 10.1093/bja/aen101.
  • Khodorova A, Montmayeur JP, Strichartz G.  (2009)  Endothelin receptors and pain.  J. Pain 10:4-28.
  • Shrestha S, Gracias N, Mujenda F, Khodorova A, Masko MR, Strichartz GR.  (2009).  Local antinociception induced by endothelin-1 in the hairy skin of the rat.  J. Pain 10:702-714.  DOI10.1016/j.jpain.2008.12.005.
  • Khodorova A, Richter J, Vasko MR, Strichartz G. (2009) Early and late contributions of glutamate and CGRP to mechanical sensitization by endothelin-1.  J. Pain 10:740-749.  DOI10.1016/j.jpain.2009.01.265.
  • Khodorova A, Zou S, Ren K, Dubner R, Davar G, Strichartz G.  (2009)  Dual roles for endothelin-B receptors in modulating adjuvant-induced inflammatory hyperalgesia in rats.  Open Pain J. 2:30-40.
  • Feng B., Strichartz G.  (2009) Endothelin-1 raises excitability and reduces potassium currents in sensory neurons.  Brain Res. Bull. 79:345-350.  DOI10.1016/j.brainresbull.2009.04.012.

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