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Role of spinal GABAA receptor reduction induced by stress in rat thermal hyperalgesia

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Abstract

The mechanisms underlying stress-induced hyperalgesia (SIH) remain poorly understood. Recent findings have provided strong evidence indicating that SIH could be related, at least in part, to alterations in spinal cord GABA activity. In the present study, we first investigated how acute restraint stress impacted pain responses as assessed using the tail flick immersion test. These results showed that rats developed hyperalgesia at 6 h after being subjected to 1-h acute restraint stress. Second, we measured the activation of spinal neurons and alterations in expression of GABAA receptor β2 and β3 subunits as related to stress-induced hyperalgesia. Results from Western blot and immunofluorescence assays showed that c-fos protein increased in the dorsal horn of the lumbar spinal cord and GABAA receptor β2 and β3 subunit proteins decreased significantly at 6 h after exposure to 1 h of acute restraint stress. Finally, the effects of spinal GABAA receptor alteration on SIH were evaluated. These results showed that intrathecal administration of muscimol inhibited hyperalgesia induced by stress while bicuculline enhanced hyperalgesia in the control groups. Taken together, the present data reveal that GABAA receptor β2 and β3 decrease following 1 h of acute restraint stress and may play a critical role in SIH.

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Acknowledgments

The study was supported by National Natural Science Foundation of China: 30800431, Shangdong Province Young and Middle-Aged Scientists Research Awards Foundation: 2011BSE27091 and China Postdoctoral Science Foundation: 2013M531616.

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There are no known conflicts of interest associated with this study.

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Correspondence to Xuelian Ma.

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Ma, X., Bao, W., Wang, X. et al. Role of spinal GABAA receptor reduction induced by stress in rat thermal hyperalgesia. Exp Brain Res 232, 3413–3420 (2014). https://doi.org/10.1007/s00221-014-4027-5

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  • DOI: https://doi.org/10.1007/s00221-014-4027-5

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