Tucker Kristal, Cavallin Melissa Ann, Jean-Baptiste Patrick, Biju K C, Overton James Michael, Pedarzani Paola, Fadool Debra Ann
Program in Neuroscience, The Florida State University, Tallahassee, FL, USA.
Results Probl Cell Differ. 2010;52:147-57. doi: 10.1007/978-3-642-14426-4_12.
The voltage-gated potassium channel, Kv1.3, contributes a large proportion of the current in mitral cell neurons of the olfactory bulb where it assists to time the firing patterns of action potentials as spike clusters that are important for odorant detection. Gene-targeted deletion of the Kv1.3 channel, produces a "super-smeller" phenotype, whereby mice are additionally resistant to diet- and genetically-induced obesity. As assessed via an electrophysiological slice preparation of the olfactory bulb, Kv1.3 is modulated via energetically important molecules - such as insulin and glucose - contributing to the body's metabolic response to fat intake. We discuss a biophysical characterization of modulated synaptic communication in the slice following acute glucose and insulin stimulation, chronic elevation of insulin in mice that are in a conscious state, and induction of diet-induced obesity. We have discovered that Kv1.3 contributes an unusual nonconducting role - the detection of metabolic state.
电压门控钾通道Kv1.3在嗅球的二尖瓣细胞神经元中贡献了很大一部分电流,它有助于将动作电位的发放模式调整为尖峰簇,这对气味检测很重要。对Kv1.3通道进行基因靶向缺失会产生“超级嗅觉者”表型,即小鼠对饮食和基因诱导的肥胖具有额外的抵抗力。通过嗅球的电生理切片制备评估发现,Kv1.3可通过能量重要分子(如胰岛素和葡萄糖)进行调节,这有助于身体对脂肪摄入的代谢反应。我们讨论了急性葡萄糖和胰岛素刺激、清醒状态小鼠胰岛素长期升高以及饮食诱导肥胖后,切片中调制突触通讯的生物物理特征。我们发现Kv1.3发挥了一种不同寻常的非传导作用——检测代谢状态。