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缺乏Kv1.1钾通道基因的小鼠的痛觉过敏

Hyperalgesia in mice lacking the Kv1.1 potassium channel gene.

作者信息

Clark J D, Tempel B L

机构信息

Department of Anesthesiology and Otolaryngology, The Virginia Merrill Bloedel Hearing Research Center, Seattle, WA 98195-7923, USA.

出版信息

Neurosci Lett. 1998 Jul 24;251(2):121-4. doi: 10.1016/s0304-3940(98)00516-3.

Abstract

Hyperalgesia and morphine induced antinociception were measured in mice lacking the gene for the Shaker-like voltage-gated potassium channel Kv1.1 alpha subunit. The effects of varying gene dosage were studied by comparing homozygous null (-/-) versus heterozygous (+/-) and wildtype (+/+) littermates. Hyperalgesia was measured using the paw flick assay, hot plate assay and formalin induced hind paw licking. It was observed that null mutant animals had significantly shorter latencies to response in the paw flick (36%) and hot plate (27%) assays while their licking times after hind paw injection of formalin was increased in both the first (74%) and second (65%) phases of the response compared to wildtype controls. Morphine induced antinociception in Kv1.1 null mutant animals was blunted. These studies indicate that Kv1.1 plays an important role in nociceptive and antinociceptive signaling pathways.

摘要

在缺乏类震颤电压门控钾通道Kv1.1α亚基基因的小鼠中测量了痛觉过敏和吗啡诱导的镇痛作用。通过比较纯合缺失(-/-)与杂合(+/-)及野生型(+/+)同窝小鼠,研究了不同基因剂量的影响。使用甩尾试验、热板试验和福尔马林诱导的后爪舔舐来测量痛觉过敏。观察到缺失突变动物在甩尾试验(36%)和热板试验(27%)中的反应潜伏期显著缩短,而与野生型对照相比,在福尔马林注射后爪后的舔舐时间在反应的第一阶段(74%)和第二阶段(65%)均增加。Kv1.1缺失突变动物中吗啡诱导的镇痛作用减弱。这些研究表明,Kv1.1在伤害性和抗伤害性信号通路中起重要作用。

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