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Lee J, Back SK, Lim EJ, et al. Are spinal GABAergic elements related to the manifestation of neuropathic pain in rat?. Korean J Physiol Pharmacol. 2010;14(2):59-69doi: 10.4196/kjpp.2010.14.2.59.
Lee, J., Back, S. K., Lim, E. J., Cho, G. C., Kim, M. A., Kim, H. J., Lee, M. H., & Na, H. S. (2010). Are spinal GABAergic elements related to the manifestation of neuropathic pain in rat?. The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 14(2), 59-69. https://doi.org/10.4196/kjpp.2010.14.2.59
Lee, Jaehee, et al. "Are spinal GABAergic elements related to the manifestation of neuropathic pain in rat?." The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology vol. 14,2 (2010): 59-69. doi: https://doi.org/10.4196/kjpp.2010.14.2.59
Lee J, Back SK, Lim EJ, Cho GC, Kim MA, Kim HJ, Lee MH, Na HS. Are spinal GABAergic elements related to the manifestation of neuropathic pain in rat?. Korean J Physiol Pharmacol. 2010 Apr;14(2):59-69. doi: 10.4196/kjpp.2010.14.2.59. Epub 2010 Apr 30. PMID: 20473376; PMCID: PMC2869462.
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Korean J Physiol Pharmacol. 2010 Apr;14(2):59-69. doi: 10.4196/kjpp.2010.14.2.59. Epub 2010 Apr 30.

Are spinal GABAergic elements related to the manifestation of neuropathic pain in rat?.

The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology

Jaehee Lee, Seung Keun Back, Eun Jeong Lim, Gyu Chong Cho, Myung Ah Kim, Hee Jin Kim, Min Hee Lee, Heung Sik Na

Affiliations

  1. Medical Science Research Center and Department of Physiology, Korea University College of Medicine, Seoul 136-705, Korea.

PMID: 20473376 PMCID: PMC2869462 DOI: 10.4196/kjpp.2010.14.2.59

Abstract

Impairment in spinal inhibition caused by quantitative alteration of GABAergic elements following peripheral nerve injury has been postulated to mediate neuropathic pain. In the present study, we tested whether neuropathic pain could be induced or reversed by pharmacologically modulating spinal GABAergic activity, and whether quantitative alteration of spinal GABAergic elements after peripheral nerve injury was related to the impairment of GABAergic inhibition or neuropathic pain. To these aims, we first analyzed the pain behaviors following the spinal administration of GABA antagonists (1 microg bicuculline/rat and 5 microg phaclofen/rat), agonists (1 microg muscimol/rat and 0.5 microg baclofen/rat) or GABA transporter (GAT) inhibitors (20 microg NNC-711/rat and 1 microg SNAP-5114/rat) into naïve or neuropathic animals. Then, using Western blotting, PCR or immunohistochemistry, we compared the quantities of spinal GABA, its synthesizing enzymes (GAD65, 67) and its receptors (GABA(A) and GABA(B)) and transporters (GAT-1, and -3) between two groups of rats with different severity of neuropathic pain following partial injury of tail-innervating nerves; the allodynic and non-allodynic groups. Intrathecal administration of GABA antagonists markedly lowered tail-withdrawal threshold in naïve animals, and GABA agonists or GAT inhibitors significantly attenuated neuropathic pain in nerve-injured animals. However, any quantitative changes in spinal GABAergic elements were not observed in both the allodynic and non-allodynic groups. These results suggest that although the impairment in spinal GABAergic inhibition may play a role in mediation of neuropathic pain, it is not accomplished by the quantitative change in spinal elements for GABAergic inhibition and therefore these elements are not related to the generation of neuropathic pain following peripheral nerve injury.

Keywords: GABA; GAD65; GAD67; GAT-1; GAT-3; Neuropathic pain; Peripheral nerve injury

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