Scott Michael M, Marcus Jacob N, Elmquist Joel K
Center for Hypothalamic Research, University of Texas Southwestern Medical Center, Dallas, 75390, USA.
Neuron. 2006 Jun 1;50(5):665-7. doi: 10.1016/j.neuron.2006.05.014.
Relatively little is known about the mechanisms that link changing levels of glucose and neuronal activity. A paper in the current issue of Neuron by Burdakov et al. demonstrates that orexin/hypocretin neurons are inhibited by rising glucose in part due to membrane potential effects mediated by tandem-pore K(+) (K(2P)) channels. The findings may shed light on the mechanisms that link hypoglycemia and coordinated arousal and autonomic responses.
关于连接葡萄糖水平变化与神经元活动的机制，我们所知相对较少。布尔达科夫等人发表在本期《神经元》杂志上的一篇论文表明，食欲素/下丘脑泌素神经元会因葡萄糖水平升高而受到抑制，部分原因是串联孔钾离子（K(2P)）通道介导的膜电位效应。这些发现可能有助于阐明将低血糖与协调性觉醒及自主反应联系起来的机制。
