下丘脑室旁核的 AVP 神经元调节摄食。
AVP neurons in the paraventricular nucleus of the hypothalamus regulate feeding.
机构信息
Department of Pediatrics, University of Michigan, Ann Arbor, MI 48109, USA.
Department of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.
出版信息
Mol Metab. 2014 Jan 8;3(2):209-15. doi: 10.1016/j.molmet.2013.12.006. eCollection 2014 Apr.
Melanocortins and their receptors are critical components of energy homeostasis and the paraventricular nucleus of the hypothalamus (PVH) is an important site of melanocortin action. Although best known for its role in osmoregulation, arginine vasopressin (AVP) has been implicated in feeding and is robustly expressed in the PVH. Since the anorectic melanocortin agonist MTII activates PVH-AVP neurons, we hypothesized that PVH-AVP neurons contribute to PVH-mediated anorexia. To test this, we used an AVP-specific Cre-driver mouse in combination with viral vectors to acutely manipulate PVH-AVP neuron function. Using designer receptors exclusively activated by designer drugs (DREADDs) to control PVH-AVP neuron activity, we show that activation of PVH-AVP neurons acutely inhibits food intake, whereas their inhibition partially reverses melanocortin-induced anorexia. We further show that MTII fails to fully suppress feeding in mice with virally-induced PVH-AVP neuron ablation. Thus PVH-AVP neurons contribute to feeding behaviors, including the acute anorectic response to MTII.
黑皮质素及其受体是能量平衡的关键组成部分，下丘脑室旁核（PVH）是黑皮质素作用的重要部位。精氨酸加压素（AVP）虽然以其在渗透压调节中的作用而闻名，但它也与摄食有关，并且在 PVH 中强烈表达。由于厌食性黑皮质素激动剂 MTII 激活 PVH-AVP 神经元，我们假设 PVH-AVP 神经元有助于 PVH 介导的厌食症。为了验证这一点，我们使用了一种特异性针对 AVP 的 Cre 驱动小鼠与病毒载体结合，以急性操纵 PVH-AVP 神经元功能。使用专门被设计药物激活的 Designer Receptors Exclusively Activated by Designer Drugs（DREADDs）来控制 PVH-AVP 神经元活性，我们发现激活 PVH-AVP 神经元可急性抑制摄食，而抑制其活性可部分逆转黑皮质素引起的厌食症。我们进一步表明，在 PVH-AVP 神经元消融的病毒诱导小鼠中，MTII 无法完全抑制摄食。因此，PVH-AVP 神经元参与摄食行为，包括对 MTII 的急性厌食反应。
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