Peer-Reviewed Journal Details
Mandatory Fields
Rea, K;Olango, WM;Okine, BN;Madasu, MK;McGuire, IC;Coyle, K;Harhen, B;Roche, M;Finn, DP
2014
January
Pain
Impaired endocannabinoid signalling in the rostral ventromedial medulla underpins genotype-dependent hyper-responsivity to noxious stimuli
Published
Altmetric: 2WOS: 32 ()
Optional Fields
ACID AMIDE HYDROLASE FEAR-CONDITIONED ANALGESIA CANNABINOID RECEPTOR AGONIST STRESS-INDUCED ANALGESIA FAAH INHIBITOR URB597 HIGH-ANXIETY RATS BRAIN-STEM MOLECULAR CHARACTERIZATION BASOLATERAL AMYGDALA INFLAMMATORY PAIN
155
69
79
Pain is both a sensory and an emotional experience, and is subject to modulation by a number of factors including genetic background modulating stress/affect. The Wistar-Kyoto (WKY) rat exhibits a stress-hyper-responsive and depressive-like phenotype and increased sensitivity to noxious stimuli, compared with other rat strains. Here, we show that this genotype-dependent hyperalgesia is associated with impaired pain-related mobilisation of endocannabinoids and transcription of their synthesising enzymes in the rostral ventromedial medulla (RVM). Pharmacological blockade of the Cannabinoid(1) (CB1) receptor potentiates the hyperalgesia in WKY rats, whereas inhibition of the endocannabinoid catabolising enzyme, fatty acid amide hydrolase, attenuates the hyperalgesia. The latter effect is mediated by CB1 receptors in the RVM. Together, these behavioural, neurochemical, and molecular data indicate that impaired endocannabinoid signalling in the RVM underpins hyper-responsivity to noxious stimuli in a genetic background prone to heightened stress/affect. (C) 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
0304-3959
10.1016/j.pain.2013.09.012
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