Moran Timothy H, Aja Susan, Ladenheim Ellen E
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Ross 618, 720 Rutland Ave., Baltimore, MD 21205, United States.
Physiol Behav. 2006 Nov 30;89(4):511-6. doi: 10.1016/j.physbeh.2006.04.020. Epub 2006 Jun 2.
Leptin reduces food intake through a specific effect on meal size. Investigations into how this within meal effect of leptin is mediated have demonstrated that leptin increases the ability of within meal inhibitory feedback signaling to limit intake and activate neurons within the nucleus of the solitary tract (NTS). Leptin's effects on neural activation can be demonstrated both as an increase in c-fos activation and as increase in electrophysiological activity in response to peripheral stimuli. Leptin can exert these effects through interactions at hypothalamic sites and activation of a descending pathway. NPY has opposite effect suggesting a role for reduced NPY signaling in the actions of leptin. Forebrain ventricular administration of a melanocortin agonist does not mimic the actions of leptin. As well as modulating within meal signaling through a descending pathway leptin, NPY and melanocortins could work directly at hindbrain integrative sites suggesting the possibility of distributed controls of meal size by anorexigenic and orexigenic signaling.
瘦素通过对进餐量的特定作用来减少食物摄入量。对瘦素这种进餐时效应的介导方式的研究表明，瘦素增强了进餐时抑制性反馈信号限制摄入量的能力，并激活了孤束核（NTS）内的神经元。瘦素对神经激活的作用既可以表现为c-fos激活的增加，也可以表现为对周围刺激的电生理活动的增加。瘦素可以通过下丘脑部位的相互作用和下行通路的激活来发挥这些作用。神经肽Y（NPY）具有相反的作用，提示NPY信号减弱在瘦素作用中发挥作用。在前脑室注射促黑素激动剂并不能模拟瘦素的作用。除了通过下行通路调节进餐时信号外，瘦素、NPY和促黑素可能直接在后脑整合部位发挥作用，提示存在由厌食信号和食欲信号对进餐量进行分布式控制的可能性。
