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Michael J. Caterina, MD, PhD

photo of Dr. Michael Catarina

Director, Neurosurgery Pain Research Institute
Professor of Neurosurgery
Professor of Biological Chemistry
Professor of Neuroscience

410-502-5457 (p)

Primary Location:
Johns Hopkins University
School of Medicine
Biophysics 408
725 North Wolfe St.
Baltimore, MD 21205


Dr. Caterina is the inaugural Director of the Johns Hopkins Neurosurgery Pain Research Institute. He is a Professor of Neurosurgery, Biological Chemistry and Neuroscience and one of the founding members of the Center for Sensory Biology. Dr. Caterina is a sensory neurobiologist with a focus on the molecular basis of pain and temperature sensation. He also leads the Johns Hopkins Medicine Brain Sciences Institute's Pain Working Group, which brings together investigators from multiple disciplines to enhance our understanding of pain mechanisms.

Dr. Caterina and his colleagues discovered the first heat-gated ion channel, the capsaicin receptor TRPV1, and demonstrated that this protein is critical for the detection of painfully hot temperatures and for the augmented sensitivity to heat pain that follows tissue inflammation. His work has been recognized with a number of national and international awards, including the Patrick Wall Young Investigator Award from the International Association for the Study of Pain in 2005 and the Donlin M. Long Pain Service Award from the Johns Hopkins Blaustein Pain Research Program in 2013.

Dr. Caterina earned his bachelor's degree from The Pennsylvania State University and subsequently the M.D. and Ph.D. degrees from the Johns Hopkins School of Medicine.

Research Summary:

TRP channel function in thermosensation, pain, and inflammation

My lab studies the biological functions and biophysical characteristics of a group of ion channel proteins of the Transient Receptor Potential Vanilloid (TRPV) family, TRPV1, TRPV2, TRPV3 and TRPV4. These channels share the intriguing feature that they can be activated by warm or painfully hot temperatures, as well as by many nonthermal stimuli. For example, TRPV1, the founding member of this family, can be activated by painful heat (>42°C), by protons, or by pungent chemicals such as capsaicin. This channel is strongly expressed in nociceptive neurons and is essential for normal behavioral responses to noxious heat. By examining these channels in recombinant and native systems, and taking advantage of knockout mice lacking one or more subtypes, we are dissecting the biological contributions of these channels to thermosensory and nonthermosensory processes in both neuronal and nonneuronal cells. We are also seeking to more broadly understand the biological and pathophysiological basis of chronic pain.

Current areas of emphasis include:

  1. Understanding the mechanisms by which TRPV1 dynamically alters its selectivity among Ca2+, Na+ and other cations during persistent stimulation, and the biological significance of this plasticity.
  2. Understanding the mechanisms by which keratinocytes in the skin contribute to “indirect” thermosensation and pain perception by signaling to epidermal nerve endings.
  3. Examination of nonthermosensory roles for TRPV channels in epithelial cells of the skin and urinary bladder, as well as other cell types.
  4. Developing novel assays and reagents for the quantification and characterization of nociception and nociceptive neurons at baseline and under chronic pain conditions.
  5. Characterizing the contributions of distinct subsets of sensory neurons to pain and hyperalgesia.

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