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首页> 外文期刊>Neuron >A Postsynaptic AMPK -> p21-Activated Kinase Pathway Drives Fasting-Induced Synaptic Plasticity in AgRP Neurons
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A Postsynaptic AMPK -> p21-Activated Kinase Pathway Drives Fasting-Induced Synaptic Plasticity in AgRP Neurons

机译：突触后的AMPK-> p21激活的激酶途径驱动空腹诱导的AgRP神经元的突触可塑性。

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摘要

AMP-activated protein kinase (AMPK) plays an important role in regulating food intake. The downstream AMPK substrates and neurobiological mechanisms responsible for this, however, are ill defined. Agouti-related peptide (AgRP)-expressing neurons in the arcuate nucleus regulate hunger. Their firing increases with fasting, and once engaged they cause feeding. AgRP neuron activity is regulated by state-dependent synaptic plasticity: fasting increases dendritic spines and excitatory synaptic activity; feeding does the opposite. The signaling mechanisms underlying this, however, are also unknown. Using neuron-specific approaches to measure and manipulate kinase activity specifically within AgRP neurons, we establish that fasting increases AMPK activity in AgRP neurons, that increased AMPK activity in AgRP neurons is both necessary and sufficient for fasting-induced spinogenesis and excitatory synaptic activity, and that the AMPK phosphorylation target mediating this plasticity is p21-activated kinase. This provides a signaling and neurobiological basis for both AMPK regulation of energy balance and AgRP neuron state-dependent plasticity.
机译：AMP激活的蛋白激酶（AMPK）在调节食物摄入中起重要作用。然而，下游的AMPK底物和神经生物学机制对此尚不明确。弓形核中表达刺痛相关肽（AgRP）的神经元调节饥饿感。他们的禁食会增加他们的射击，一旦交战就会引起进食。 AgRP神经元活性受状态依赖性突触可塑性调节：禁食可增加树突棘和兴奋性突触活性;喂养则相反。然而，基于此的信号传导机制也是未知的。使用特定于神经元的方法来测量和操纵AgRP神经元内的激酶活性，我们确定禁食可增加AgRP神经元中的AMPK活性，而增加AgRP神经元中的AMPK活性对于禁食诱导的纺丝原性和兴奋性突触活性既必要又充分。介导这种可塑性的AMPK磷酸化目标是p21激活的激酶。这为AMPK调节能量平衡和AgRP神经元状态依赖性可塑性提供了信号和神经生物学基础。

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