Spinal endocannabinoids and CB1 receptors mediate C-fiber-induced heterosynaptic pain sensitization. Science (New York, N.Y.) [Science] Journal article

Title	Spinal endocannabinoids and CB1 receptors mediate C-fiber-induced heterosynaptic pain sensitization.
Author(s)	Pernía-Andrade AJ, Kato A, Witschi R, Nyilas R, Katona I, Freund TF, Watanabe M, Filitz J, Koppert W, Schüttler J, Ji G, Neugebauer V, Marsicano G, Lutz B, Vanegas H, Zeilhofer HU
Institution	Institute of Pharmacology and Toxicology, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.
Source	Science 2009 Aug 7; 325(5941):760-4.
MeSH	Adult Animals Electric Stimulation Endocannabinoids Excitatory Postsynaptic Potentials Female Humans Hyperalgesia Inhibitory Postsynaptic Potentials Interneurons Male Mice Mice, Inbred C57BL Mice, Transgenic Nerve Fibers, Unmyelinated Neural Inhibition Pain Piperidines Posterior Horn Cells Pyrazoles Rats Rats, Sprague-Dawley Receptor, Cannabinoid, CB1 Spinal Cord Synaptic Transmission Young Adult
Abstract	Diminished synaptic inhibition in the spinal dorsal horn is a major contributor to chronic pain. Pathways that reduce synaptic inhibition in inflammatory and neuropathic pain states have been identified, but central hyperalgesia and diminished dorsal horn synaptic inhibition also occur in the absence of inflammation or neuropathy, solely triggered by intense nociceptive (C-fiber) input to the spinal dorsal horn. We found that endocannabinoids, produced upon strong nociceptive stimulation, activated type 1 cannabinoid (CB1) receptors on inhibitory dorsal horn neurons to reduce the synaptic release of gamma-aminobutyric acid and glycine and thus rendered nociceptive neurons excitable by nonpainful stimuli. Our results suggest that spinal endocannabinoids and CB1 receptors on inhibitory dorsal horn interneurons act as mediators of heterosynaptic pain sensitization and play an unexpected role in dorsal horn pain-controlling circuits.
Language	eng
Pub Type(s)	Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't
PubMed ID	19661434

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