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首页> 外文期刊>American Journal of Physiology >Brain stem melanocortinergic modulation of meal size and identification of hypothalamic POMC projections.
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Brain stem melanocortinergic modulation of meal size and identification of hypothalamic POMC projections.

机译：进餐量的脑干黑皮质素能调制和下丘脑POMC投射的鉴定。

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Metabolic, cognitive, and environmental factors processed in the forebrain modulate food intake by changing the potency of direct controls of meal ingestion in the brain stem. Here, we behaviorally and anatomically test the role of the hypothalamic proopiomelanocortin (POMC) system in mediating some of these descending, indirect controls. Melanotan II (MTII), a stable melanocortin 4 receptor (MC4R) and melanocortin 3 receptor (MC3R) agonist injected into the fourth ventricle near the dorsal vagal complex, potently inhibited 14-h food intake by decreasing meal size but not meal frequency; SHU9119, an antagonist, increased food intake by selectively increasing meal size. Furthermore, MTII injected into the fourth ventricle increased and SHU9119 tended to decrease heart rate and body temperature measured telemetrically in freely moving rats. Numerous alpha-melanocyte-stimulating hormone-immunoreactive axons were in close anatomical apposition to nucleus tractus solitarius neurons showing c-Fos in responseto gastric distension, expressing neurochemical phenotypes implicated in ingestive control, and projecting to brown adipose tissue. In retrograde tracing experiments, a small percentage of arcuate nucleus POMC neurons was found to project to the dorsal vagal complex. Thus melanocortin signaling in the brain stem is sufficient to alter food intake via changing the potency of satiety signals and to alter sympathetic outflow. Although the anatomical findings support the involvement of hypothalamomedullary POMC projections in mediating part of the descending, indirect signal, they do not rule out involvement of POMC neurons in the nucleus tractus solitarius in mediating part of the direct signal.
机译：前脑中处理的代谢，认知和环境因素通过改变直接控制膳食进食脑干的能力来调节食物摄入。在这里，我们从行为上和解剖上测试了下丘脑的proopiomelanocortin（POMC）系统在介导这些下降的间接控制中的作用。 Melanotan II（MTII）是一种稳定的melanocortin 4受体（MC4R）和melanocortin 3受体（MC3R）激动剂，被注射到背迷走神经复合体附近的第四脑室，通过减少进餐量而不是进餐频率来有效地抑制14小时进食。拮抗剂SHU9119通过选择性增加进餐量来增加食物摄入量。此外，在自由运动大鼠中，遥测的第四心室中注射的MTII升高，SHU9119趋于降低心率和体温。许多刺激α-黑素细胞的激素免疫反应性轴突在解剖上与孤立的孤核中枢神经元并列，显示响应胃扩张的c-Fos，表达了与饮食控制有关的神经化学表型，并投射到棕色脂肪组织。在逆行追踪实验中，发现一小部分弓形核POMC神经元投射到背迷走神经复合体。因此，脑干中的黑皮质素信号传导足以通过改变饱腹感信号的效力来改变食物摄入并改变交感神经。尽管解剖学发现支持下丘脑髓质POMC投射参与介导部分下降的间接信号，但它们并不排除POMC神经元参与孤束核介导部分直接信号。

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