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Leptin does not directly affect CNS serotonin neurons to influence appetite.

机译:瘦素不会直接影响中枢神经系统5-羟色胺神经元的食欲。

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摘要

Serotonin (5-HT) and leptin play important roles in the modulation of energy balance. Here we investigated mechanisms by which leptin might interact with CNS 5-HT pathways to influence appetite. Although some leptin receptor (LepRb) neurons lie close to 5-HT neurons in the dorsal raphe (DR), 5-HT neurons do not express LepRb. Indeed, while leptin hyperpolarizes some non-5-HT DR neurons, leptin does not alter the activity of DR 5-HT neurons. Furthermore, 5-HT depletion does not impair the anorectic effects of leptin. The serotonin transporter-cre allele (Sert(cre)) is expressed in 5-HT (and developmentally in some non-5-HT) neurons. While Sert(cre) promotes LepRb excision in a few LepRb neurons in the hypothalamus, it is not active in DR LepRb neurons, and neuron-specific Sert(cre)-mediated LepRb inactivation in mice does not alter body weight or adiposity. Thus, leptin does not directly influence 5-HT neurons and does not meaningfully modulate important appetite-related determinants via 5-HT neuron function.
机译:血清素(5-HT)和瘦素在调节能量平衡中起重要作用。在这里,我们研究了瘦素可能与中枢神经系统5-HT途径相互作用以影响食欲的机制。尽管一些瘦蛋白受体(LepRb)神经元在背缝(DR)中位于5-HT神经元附近,但5-HT神经元不表达LepRb。确实,尽管瘦素使某些非5-HT DR神经元超极化,但瘦素不会改变DR 5-HT神经元的活性。此外,5-HT耗竭不损害瘦素的厌食作用。血清素转运蛋白-cre等位基因(Sert(cre))在5-HT(并且在某些非5-HT)神经元中表达。尽管Sert(cre)促进下丘脑中少数LepRb神经元的LepRb切除,但它在DR LepRb神经元中不起作用,并且神经元特异性Sert(cre)介导的LepRb灭活不会改变体重或肥胖。因此,瘦素不会直接影响5-HT神经元,也不会通过5-HT神经元功能有意义地调节重要的食欲相关决定因素。

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