迈巴赫普尔曼价格:翻译(有分吆,翻译的好还加分呢???!!我有的是分)

Transduction of adiposity signals into a neuronal response Situated adjacent to the floor of the third ventricle, the arcuate nucleus is an elongate (‘arc-like’) collection of neuronal cell bodies occupying approximately one-half of the length of the hypothalamus.NPYandAGRPareco-localizedinarcuatenucleusneurons60,61, demonstrating that a single neuronal cell type can contain multiple anaboliceffectormolecules.ThesubsequentfindingthatPOMCand CART are co-localized in a distinct, but adjacent, subset of arcuate nucleusneurons66indicatesthatcircuitsoriginatinginthisbrainarea have highly specialized roles in energy homeostasis (Fig. 4). The hypothesis that the arcuate nucleus transduces information related to signalling by leptin into a neuronal response is supported by the anorexic response to local microinjection of leptin into this area67, and the inability of i.c.v. leptin to reduce food intake after the arcuate nucleus has been destroyed68,69. A majority of both NPY/AGRP and POMC/CART neurons have been found to coexpress leptin receptors16,17 and both types of neurons are regulated byleptin(asjudgedbychangesinneuropeptidegeneexpression),but in an opposing manner. Thus, NPY/AGRP neurons are inhibited by leptin,andconsequentlyareactivatedinconditionswhereleptinlevels are low44,45,60,61. Although less well studied, a deficiency of insulin also seems to activate these neurons20,47, and insulin receptors are highly concentrated in the arcuate nucleus15. Conversely, conditions characterized by reduced insulin or leptin inhibit POMC70,71 and CART52 expression in the arcuate nucleus, and administration of these hormones can prevent or attenuate these neuropeptide responses.Moreover,involuntaryoverfeedinginrats,whichpotently inhibits spontaneous food intake once body weight has increased by more than 5%, elicits a threefold increase of POMC messenger RNA levels in the arcuate nucleus72. The demonstration that anorexia induced either by leptin73 or by involuntary overfeeding72 is reversed by central administration of a melanocortin-receptor antagonist (at a low dose that has no effect on food intake in control animals) indicates that melanocortin signalling is a mediator of the anorexic response induced by increased adiposity signalling to the brain. Taken together, these findings indicate that the arcuate nucleus is a major site for transducing afferent input from circulating leptin and insulin into a neuronal response