Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-20139
Pernía-Andrade, A J; Kato, A; Witschi, R; Nyilas, R; Katona, I; Freund, T F; Watanabe, M; Filitz, J; Koppert, W; Schüttler, J; Ji, G; Neugebauer, V; Marsicano, G; Lutz, B; Vanegas, H; Zeilhofer, H U (2009). Spinal endocannabinoids and CB1 receptors mediate C-fiber-induced heterosynaptic pain sensitization. Science, 325(5941):760-764.
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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.
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > Institute of Pharmacology and Toxicology|
|DDC:||570 Life sciences; biology|
610 Medicine & health
|Date:||07 August 2009|
|Deposited On:||11 Aug 2009 11:31|
|Last Modified:||28 Nov 2013 01:48|
|Publisher:||American Association for the Advancement of Science (AAAS)|
|Free access at:||Official URL. An embargo period may apply.|
|Citations:||Web of Science®. Times cited: 50|
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