Roy Ben-Shalom

Highlights • Conditional deletion of NaV1.2 channels increases action potential (AP) excitability • NaV1.2 regulates somatodendritc excitability, and NaV1.6 regulates axonal action potential initiation • Lack of NaV1.2 channels impairs AP repolarization by reducing KV activation • Reduced KV-mediated AP after hyperpolarization increases AP output Summary Loss-of-function variants in the gene SCN2A, which encodes the sodium channel NaV1.2, are strongly associated with autism spectrum disorder...

Ariav G. Polsky A. Schiller J. Submillisecond precision of the input-output transformation function mediated by fast sodium dendritic spikes in basal dendrites of CA1 pyramidal neurons. J. Neurosci. 2003; 23: 7750-7758 Barth A.M.I. Vizi E.S. Zelles T. Lendvai B. α2-adrenergic receptors modify dendritic spike generation via HCN channels in the prefrontal cortex. J. Neurophysiol.