Division of Biology 156-29, California Institute of Technology, Pasadena, CA 91125, USA.
Proc Natl Acad Sci U S A. 2012 Mar 6;109(10):3967-72. doi: 10.1073/pnas.1200778109. Epub 2012 Feb 15.
How the brain translates changes in internal metabolic state or perceived food quality into alterations in feeding behavior remains poorly understood. Studies in Drosophila larvae have yielded information about neuropeptides and circuits that promote feeding, but a peptidergic neuron subset whose activation inhibits feeding in adult flies, without promoting metabolic changes that mimic the state of satiety, has not been identified. Using genetically based manipulations of neuronal activity, we show that activation of neurons (or neuroendocrine cells) expressing the neuropeptide allatostatin A (AstA) inhibits or limits several starvation-induced changes in feeding behavior in adult Drosophila, including increased food intake and enhanced behavioral responsiveness to sugar. Importantly, these effects on feeding behavior are observed in the absence of any measurable effects on metabolism or energy reserves, suggesting that AstA neuron activation is likely a consequence, not a cause, of metabolic changes that induce the state of satiety. These data suggest that activation of AstA-expressing neurons promotes food aversion and/or exerts an inhibitory influence on the motivation to feed and implicate these neurons and their associated circuitry in the mechanisms that translate the state of satiety into alterations in feeding behavior.
大脑如何将内部代谢状态或感知到的食物质量的变化转化为进食行为的改变，目前仍知之甚少。在果蝇幼虫中的研究已经提供了关于促进进食的神经肽和回路的信息，但尚未鉴定出一种能激活而不促进模拟饱腹感状态的代谢变化的、能抑制成蝇进食的肽能神经元亚群。利用基于遗传的神经元活性操作，我们发现表达神经肽 allatostatin A (AstA) 的神经元（或神经内分泌细胞）的激活抑制或限制了成年果蝇中几种饥饿诱导的进食行为变化，包括增加食物摄入和增强对糖的行为反应性。重要的是，在没有任何可衡量的代谢或能量储备变化的情况下观察到这些对进食行为的影响，这表明 AstA 神经元的激活可能是诱导饱腹感的代谢变化的结果，而不是原因。这些数据表明，激活表达 AstA 的神经元会促进食物厌恶和/或对进食的动机产生抑制影响，并暗示这些神经元及其相关回路参与了将饱腹感状态转化为进食行为改变的机制。
