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内源性去甲肾上腺素能张力控制神经病理性疼痛脊髓神经结扎模型中的痛觉过敏症状。

Endogenous noradrenergic tone controls symptoms of allodynia in the spinal nerve ligation model of neuropathic pain.

作者信息

Xu M, Kontinen V K, Kalso E

机构信息

Department of Pharmacology and Toxicology, Institute of Biomedicine, University of Helsinki, Finland.

出版信息

Eur J Pharmacol. 1999 Jan 29;366(1):41-5. doi: 10.1016/s0014-2999(98)00910-8.

Abstract

Endogenous inhibitory controls were studied in the spinal nerve ligation model of neuropathic pain. Atipamezole, a selective alpha2-adrenoceptor antagonist, produced both mechanical and cold allodynia in those rats which had not developed clear neuropathic symptoms. The same doses (50 microg i.t. or 1 mg/kg s.c.) did not increase the severity of symptoms in rats which had developed them. The opioid receptor antagonist naloxone (20 microg i.t. or 1 mg/kg s.c.) had no effect on the neuropathic symptoms. These results indicate that mechanical and cold allodynia are under endogenous noradrenergic rather than opioidergic control in this model of neuropathic pain.

摘要

在神经性疼痛的脊神经结扎模型中研究了内源性抑制控制。阿替美唑是一种选择性α2-肾上腺素能受体拮抗剂,在尚未出现明显神经性症状的大鼠中产生了机械性和冷觉异常性疼痛。相同剂量(鞘内注射50微克或皮下注射1毫克/千克)并未加重已出现神经性症状大鼠的症状严重程度。阿片受体拮抗剂纳洛酮(鞘内注射20微克或皮下注射1毫克/千克)对神经性症状没有影响。这些结果表明,在该神经性疼痛模型中,机械性和冷觉异常性疼痛受内源性去甲肾上腺素能而非阿片样物质能的控制。

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