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Eating disorder and epilepsy in mice lacking 5-HT2c serotonin receptors.

机译:缺乏5-HT2c血清素受体的小鼠的饮食失调和癫痫病。

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Serotonin (5-hydroxytryptamine, 5-HT) is a monoaminergic neurotransmitter that is believed to modulate numerous sensory, motor and behavioural processes in the mammalian nervous system. These diverse responses are elicited through the activation of a large family of receptor subtypes. The complexity of this signalling system and the paucity of selective drugs have made it difficult to define specific roles for 5-HT receptor subtypes, or to determine how serotonergic drugs modulate mood and behaviour. To address these issues, we have generated mutant mice lacking functional 5-HT2C receptors (previously termed 5-HT1C), prominent G-protein-coupled receptors that are widely expressed throughout the brain and spinal cord and which have been proposed to mediate numerous central nervous system (CNS) actions of serotonin. Here we show that 5-HT2C receptor-deficient mice are overweight as a result of abnormal control of feeding behaviour, establishing a role for this receptor in the serotonergic control of appetite. Mutant animals are also prone to spontaneous death from seizures, suggesting that 5-HT2C receptors mediate tonic inhibition of neuronal network excitability.
机译:5-羟色胺(5-羟色胺,5-HT)是一种单胺能神经递质,据信可调节哺乳动物神经系统的许多感觉,运动和行为过程。这些不同的反应是通过激活一大批受体亚型引起的。该信号系统的复杂性和选择性药物的匮乏使得很难定义5-HT受体亚型的特定作用,或确定血清素能药物如何调节情绪和行为。为了解决这些问题,我们已经产生了缺乏功能性5-HT2C受体(以前称为5-HT1C),显着的G蛋白偶联受体的突变小鼠,该受体在脑和脊髓中广泛表达,并且已提出介导许多中枢神经系统血清素对神经系统(CNS)的作用。在这里,我们显示5-HT2C受体缺陷型小鼠由于进食行为的异常控制而超重,从而确立了该受体在食欲的血清素能控制中的作用。突变的动物也容易因癫痫发作而自发死亡,这表明5-HT2C受体介导了对神经元网络兴奋性的强直抑制作用。

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