Epilepsy and obesity in serotonin 5-HT2C receptor mutant mice
Epilepsy and obesity in serotonin 5-HT2C receptor mutant mice
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DOI：
10.1111/j.1749-6632.1998.tb10175.x
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发表时间：
1998-01-01
期刊：
影响因子：
--
通讯作者：
Tecott, LH
中科院分区：
文献类型：
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作者：
Heisler, LK;Chu, HM;Tecott, LH
产生5-羟色胺5-HT 2C受体无效突变小鼠以评估该受体对5-羟色胺作用的贡献。突变小鼠显示癫痫和肥胖表型。癫痫综合征以自发性癫痫发作为特征。降低癫痫发作阈值，增强癫痫发作传播和声音诱发的癫痫发作易感性，这些发现暗示5-HT 2C受体参与神经网络兴奋性的调节。还观察到，相对于其野生型同窝出生小鼠，成年突变小鼠的体重和脂肪组织沉积升高。配对喂养研究表明，肥胖综合征是食物摄入量增加的结果。此外，突变体显示对非特异性多巴胺能激动剂的食欲抑制作用的敏感性降低。这些研究确立了5-HT 2C受体在多巴胺能调节体重和食物摄入中的作用。
Serotonin 5-HT2C receptor null mutant mice were generated to assess the contribution of this receptor to the actions of serotonin, Mutant mice displayed both an epilepsy and obesity phenotype. The epilepsy syndrome was characterized by spontaneous seizures. lowered seizure threshold, enhanced seizure propagation and sound-induced seizure susceptibility, These findings implicate 5-HT2C receptors in the regulation of neuronal network excitability. It was also observed that body weight and adipose tissue deposition were elevated in adult mutant mice relative to their wild type littermates. Paired-feeding studies suggest that the obesity syndrome is a result of increased food intake. In addition, mutants displayed reduced sensitivity to the appetite suppressant actions of nonspecific serotonergic agonists, These studies establish a role for 5-HT2C receptors in the serotonergic regulation of body weight and food intake.