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Pain-related behavior following REM sleep deprivation in the rat: influence of peripheral nerve injury, spinal glutamatergic receptors and nitric oxide.
Brain Res. 2007 May 07; 1148:105-12.BR

Abstract

We assessed whether pain-related behavior in neuropathic or control rats is changed following rapid eye movement sleep deprivation (REMSD). Furthermore, we determined the contribution of spinal glutamatergic receptors and nitric oxide to sensitivity changes following REMSD versus peripheral nerve injury. Pain behavior was assessed in Sprague-Dawley (SD) and Hannover-Wistar (HW) rats with a spinal nerve ligation or a sham operation. Nerve ligation produced mechanical hypersensitivity of the injured dermatome in all animals. Baseline sensitivity to mechanical stimulation was higher in the HW than the SD group, independent of nerve injury. In both strains, mechanical sensitivity of neuropathic and sham-operated animals was increased following 48 h of REMSD. Heat sensitivity of an uninjured dermatome was not different among experimental conditions. Reversal of mechanical hypersensitivity was attempted in HW rats by spinal administration of an antagonist of the metabotropic glutamate receptor 5 (mGluR(5)) or the NMDA receptor and a nitric oxide synthase (NOS) inhibitor. Mechanical hypersensitivity induced by REMSD in unoperated rats was attenuated by all three drugs, while in neuropathic animals the mechanical anti-hypersensitive effect was most pronounced with the antagonist of the mGluR(5) or a NOS inhibitor. The results indicate that the strain of the animals markedly influences baseline withdrawal threshold to mechanical stimulation. Mechanical hypersensitivity following REMSD, however, is similarly increased in HW and SD strains, and the REMSD-associated increase in mechanical sensitivity is independent of nerve injury. Furthermore, mechanical hypersensitivities following REMSD and peripheral nerve injury share common spinal mechanisms involving, at least, the mGluR(5) and nitric oxide.

Authors+Show Affiliations

School of Pharmacy, Shanghai Jiao Tong University, Dongchuan Road 800, Shanghai 200240, China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17368427

Citation

Wei, Hong, et al. "Pain-related Behavior Following REM Sleep Deprivation in the Rat: Influence of Peripheral Nerve Injury, Spinal Glutamatergic Receptors and Nitric Oxide." Brain Research, vol. 1148, 2007, pp. 105-12.
Wei H, Zhao W, Wang YX, et al. Pain-related behavior following REM sleep deprivation in the rat: influence of peripheral nerve injury, spinal glutamatergic receptors and nitric oxide. Brain Res. 2007;1148:105-12.
Wei, H., Zhao, W., Wang, Y. X., & Pertovaara, A. (2007). Pain-related behavior following REM sleep deprivation in the rat: influence of peripheral nerve injury, spinal glutamatergic receptors and nitric oxide. Brain Research, 1148, 105-12.
Wei H, et al. Pain-related Behavior Following REM Sleep Deprivation in the Rat: Influence of Peripheral Nerve Injury, Spinal Glutamatergic Receptors and Nitric Oxide. Brain Res. 2007 May 7;1148:105-12. PubMed PMID: 17368427.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pain-related behavior following REM sleep deprivation in the rat: influence of peripheral nerve injury, spinal glutamatergic receptors and nitric oxide. AU - Wei,Hong, AU - Zhao,Wenjuan, AU - Wang,Yong-Xiang, AU - Pertovaara,Antti, Y1 - 2007/02/24/ PY - 2006/10/25/received PY - 2007/01/26/revised PY - 2007/02/15/accepted PY - 2007/3/21/pubmed PY - 2007/7/26/medline PY - 2007/3/21/entrez SP - 105 EP - 12 JF - Brain research JO - Brain Res VL - 1148 N2 - We assessed whether pain-related behavior in neuropathic or control rats is changed following rapid eye movement sleep deprivation (REMSD). Furthermore, we determined the contribution of spinal glutamatergic receptors and nitric oxide to sensitivity changes following REMSD versus peripheral nerve injury. Pain behavior was assessed in Sprague-Dawley (SD) and Hannover-Wistar (HW) rats with a spinal nerve ligation or a sham operation. Nerve ligation produced mechanical hypersensitivity of the injured dermatome in all animals. Baseline sensitivity to mechanical stimulation was higher in the HW than the SD group, independent of nerve injury. In both strains, mechanical sensitivity of neuropathic and sham-operated animals was increased following 48 h of REMSD. Heat sensitivity of an uninjured dermatome was not different among experimental conditions. Reversal of mechanical hypersensitivity was attempted in HW rats by spinal administration of an antagonist of the metabotropic glutamate receptor 5 (mGluR(5)) or the NMDA receptor and a nitric oxide synthase (NOS) inhibitor. Mechanical hypersensitivity induced by REMSD in unoperated rats was attenuated by all three drugs, while in neuropathic animals the mechanical anti-hypersensitive effect was most pronounced with the antagonist of the mGluR(5) or a NOS inhibitor. The results indicate that the strain of the animals markedly influences baseline withdrawal threshold to mechanical stimulation. Mechanical hypersensitivity following REMSD, however, is similarly increased in HW and SD strains, and the REMSD-associated increase in mechanical sensitivity is independent of nerve injury. Furthermore, mechanical hypersensitivities following REMSD and peripheral nerve injury share common spinal mechanisms involving, at least, the mGluR(5) and nitric oxide. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/17368427/Pain_related_behavior_following_REM_sleep_deprivation_in_the_rat:_influence_of_peripheral_nerve_injury_spinal_glutamatergic_receptors_and_nitric_oxide_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(07)00430-1 DB - PRIME DP - Unbound Medicine ER -