Engbers, Jordan D .T.Anderson, Dustin M.Asmara, HadhimulyaRehak, RenataMehaffey, W. HamishHameed, ShahidMcKay, Bruce E.Kruskic, MirnaZamponi, Gerald W.Turner, Ray W.2018-05-222018-05-222012-02-14Engbers, J. D. T., Anderson, D., Asmara, H., Rehak, R., Mehaffey, W. H., Hameed, S., … Turner, R. W. (2012). Intermediate conductance calcium-activated potassium channels modulate summation of parallel fiber input in cerebellar Purkinje cells. Proceedings of the National Academy of Sciences, 109(7), 2601–2606. https://doi.org/10.1073/pnas.1115024109http://hdl.handle.net/1880/106649https://doi.org/10.11575/PRISM/43842Encoding sensory input requires the expression of postsynaptic ion channels to transform key features of afferent input to an appropriate pattern of spike output. Although Ca(2+)-activated K(+) channels are known to control spike frequency in central neurons, Ca(2+)-activated K(+) channels of intermediate conductance (KCa3.1) are believed to be restricted to peripheral neurons. We now report that cerebellar Purkinje cells express KCa3.1 channels, as evidenced through single-cell RT-PCR, immunocytochemistry, pharmacology, and single-channel recordings. Furthermore, KCa3.1 channels coimmunoprecipitate and interact with low voltage-activated Cav3.2 Ca(2+) channels at the nanodomain level to support a previously undescribed transient voltage- and Ca(2+)-dependent current. As a result, subthreshold parallel fiber excitatory postsynaptic potentials (EPSPs) activate Cav3 Ca(2+) influx to trigger a KCa3.1-mediated regulation of the EPSP and subsequent after-hyperpolarization. The Cav3-KCa3.1 complex provides powerful control over temporal summation of EPSPs, effectively suppressing low frequencies of parallel fiber input. KCa3.1 channels thus contribute to a high-pass filter that allows Purkinje cells to respond preferentially to high-frequency parallel fiber bursts characteristic of sensory input.enjournal articlehttp://dx.doi.org/10.1073/pnas.1115024109