Alla Khodorova1, 8, Betsy Navarro2, 8, Laurence Sophie Jouaville1, 3, 8, Jo-Ellen Murphy4, Frank L Rice5, Joseph E Mazurkiewicz5, Denise Long-Woodward4, Markus Stoffel6, Gary R Strichartz3, Rus Yukhananov7
& Gudarz Davar11
Molecular Neurobiology of Pain Laboratory, Pain Research Center, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, 02115 USA.
2
Department of Cardiology, Children's Hospital, Harvard Medical School, Boston, Massachusetts, 02115 USA.
3
Sensory Neurophysiology Laboratory, Pain Research Center, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School Boston, Massachusetts, 02115 USA.
4
Harvard Skin Disease Research Center, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, 02115 USA.
5
Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, New York, 12208 USA.
6
Laboratory of Metabolic Diseases, Rockefeller University, New York, New York, 10021 USA.
7
Neurogenomic Laboratory, Pain Research Center, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, 02115 USA.
8
These authors contributed equally to this work.
Correspondence should be addressed to Gudarz Davar gdavar@zeus.bwh.harvard.edu
-endorphin from keratinocytes and the activation of G-protein-coupled inwardly rectifying potassium channels (GIRKs, also named Kir-3) linked to opioid receptors on nociceptors. These results indicate the existence of an intrinsic feedback mechanism to control peripheral pain in skin, and establish keratinocytes as an ETB receptor−operated opioid pool.
