Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA, USA.
Department of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Nat Commun. 2021 Apr 9;12(1):2135. doi: 10.1038/s41467-021-22430-7.
Hedonic feeding is driven by the "pleasure" derived from consuming palatable food and occurs in the absence of metabolic need. It plays a critical role in the excessive feeding that underlies obesity. Compared to other pathological motivated behaviors, little is known about the neural circuit mechanisms mediating excessive hedonic feeding. Here, we show that modulation of prefrontal cortex (PFC) and anterior paraventricular thalamus (aPVT) excitatory inputs to the nucleus accumbens (NAc), a key node of reward circuitry, has opposing effects on high fat intake in mice. Prolonged high fat intake leads to input- and cell type-specific changes in synaptic strength. Modifying synaptic strength via plasticity protocols, either in an input-specific optogenetic or non-specific electrical manner, causes sustained changes in high fat intake. These results demonstrate that input-specific NAc circuit adaptations occur with repeated exposure to a potent natural reward and suggest that neuromodulatory interventions may be therapeutically useful for individuals with pathologic hedonic feeding.
享乐性进食是由食用美味食物所带来的“愉悦”驱动的，发生在没有代谢需求的情况下。它在肥胖症的过度进食中起着关键作用。与其他病理性动机行为相比，人们对介导过度享乐性进食的神经回路机制知之甚少。在这里，我们表明，调节前额叶皮层（PFC）和前室旁丘脑（aPVT）对伏隔核（NAc）的兴奋性输入，NAc 是奖励回路的关键节点，对小鼠的高脂肪摄入有相反的影响。长期高脂肪摄入会导致突触强度的输入和细胞类型特异性变化。通过可塑性方案改变突触强度，无论是特定于输入的光遗传学还是非特异性的电方式，都会导致高脂肪摄入的持续变化。这些结果表明，随着反复接触强效天然奖励，NAc 电路会发生特定于输入的适应性改变，并表明神经调节干预可能对病理性享乐性进食的个体具有治疗作用。
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