• Juan-Xia Zhu, Feng-Yi Xu, Wen-Jin Xu, Yan Zhao, Chao-Ling Qu, Jing-Shi Tang, Devin M Barry, Jian-Qing Du, and Fu-Quan Huo.
• Department of Physiology and Pathophysiology, Xi'an Jiaotong University College of Medicine, Yanta Road W. 76#, Xi'an, Shaanxi 710061, PR China; Department of Physiology, Xi'an Medical University, Xinwang Road 1#, Xi'an, Shaanxi 710021, PR China.
• Exp. Neurol. 2013 Oct 1; 248: 381-6.

AbstractThe present study examined the role of α₂ adrenoceptor in mediating noradrenaline action in the ventrolateral orbital cortex (VLO) on allodynia induced by spared nerve injury (SNI) in the rat. The mechanical paw withdrawal threshold (PWT) was measured using von-Frey filaments. Microinjection of noradrenaline (1, 2, 4 μg in 0.5 μl) into the VLO, contralateral to the site of nerve injury, reduced allodynia; PWT increased in a dose-dependent manner. Similar to noradrenaline, microinjection of selective α₂ adrenoceptor agonist clonidine into the same VLO site also reduced allodynia, and was blocked by selective α₂ adrenoceptor antagonist yohimbine. Furthermore, administration of γ-aminobutyric acid A (GABAA) receptor antagonist bicuculline or picrotoxin to the VLO significantly enhanced clonidine-induced inhibition of allodynia, while GABAA receptor agonist muscimol or THIP (2,5,6,7-retrahydroisoxazolo(5,4-c)pyridine-3-ol hydrochloride) attenuated clonidine-induced inhibition. These results suggest that noradrenaline acting in the VLO can potentially reduce allodynia induced by SNI, and this effect is mediated by α₂ adrenoceptor. Moreover, GABAergic disinhibition may participate in α₂ receptor mediating effects in neuropathic pain in the central nervous system.© 2013.

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