PDF(Pubmed)
Abstract：
Efficient control of feeding behavior requires the coordinated adjustment of complex motivational and affective neurocircuits. Neuropeptides from energy-sensing hypothalamic neurons are potent feeding modulators, but how these endogenous signals shape relevant circuits remains unclear. Here, we examine how the orexigenic neuropeptide Y (NPY) adapts GABAergic inputs to the bed nucleus of the stria terminalis (BNST). We find that fasting increases synaptic connectivity between agouti-related peptide (AgRP)-expressing \'hunger\' and BNST neurons, a circuit that promotes feeding. In contrast, GABAergic input from the central amygdala (CeA), an extended amygdala circuit that decreases feeding, is reduced. Activating NPY-expressing AgRP neurons evokes these synaptic adaptations, which are absent in NPY-deficient mice. Moreover, fasting diminishes the ability of CeA projections in the BNST to suppress food intake, and NPY-deficient mice fail to decrease anxiety in order to promote feeding. Thus, AgRP neurons drive input-specific synaptic plasticity, enabling a selective shift in hunger and anxiety signaling during starvation through NPY.
摘要：
喂养行为的有效控制需要复杂的动机和情感神经回路的协调调整。来自能量感应下丘脑神经元的神经肽是有效的摄食调节剂，但这些内源性信号如何塑造相关电路仍不清楚。这里,我们研究了生性神经肽Y（NPY）如何将GABA能输入适应终末纹（BNST）的床核。我们发现禁食会增加表达“饥饿”相关肽（AgRP）和BNST神经元之间的突触连接，促进进食的电路。相比之下,来自中央杏仁核（CeA）的GABA能输入，延长杏仁核回路，减少进食，减少了。激活NPY表达的AgRP神经元唤起这些突触适应，在缺乏NPY的小鼠中不存在。此外，禁食会降低BNST中CeA投影抑制食物摄入的能力，和缺乏NPY的小鼠不能减少焦虑以促进喂养。因此，AgRP神经元驱动输入特异性突触可塑性，在饥饿期间通过NPY实现饥饿和焦虑信号的选择性转变。
