Visinin-like neuronal calcium sensor proteins regulate the slow calcium-activated afterhyperpolarizing current in the rat cerebral cortex.
In hippocampal pyramidal neurons, calcium entry following an action potential burst results in a slow afterhyperpolarization (sAHP) that critically regulates subsequent excitability. Although this potassium current was described two decades ago, the mechanism whereby the rise in intracellular calcium generates the sAHP was, until now, not known. In this issue of Neuron, Tzingounis et al. now show that calcium binding to hippocalcin, a member of the NCS family, is one of the necessary steps involved in production of the sAHP.