Calcium Regulation of a Slow AHP in Hippocampal Pyramidal Cells
Date
2018-04-12
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Abstract
A slow afterhyperpolarization (sAHP) in CA1 hippocampal pyramidal cells is calcium-dependent and involves activation of KCa3.1 and KCNQ potassium channels. Both KCa3.1 and KCNQ channels bind calmodulin (CaM) as a calcium sensor, with an additional role proposed for the protein hippocalcin. We measured the calcium sensitivity of the IsAHP and potassium channel associations with CaM or hipppocalcin. In recordings in hippocampal tissue slices in vitro the KCa3.1-mediated IsAHP steadily increased over 10 min equilibration to 0 µM calcium electrolyte, but decreased upon infusing 1 µM calcium, while the KCNQ-mediated IsAHP responded in an opposite manner. KCa3.1 channels contributed to the IsAHP in rat but not mouse pyramidal cells. Coimmunoprecipitation occurred between KCa3.1 and both CaM and hippocalcin, but only KCNQ and CaM. These data reveal a species-specific expression pattern for two potassium channels and in calcium sensor proteins present to generate the sAHP in the same class of hippocampal neuron.
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Keywords
slow afterhyperpolarization, hippocampus, CA1, hippocalcin, calmodulin, KCa3.1, KCNQ
Citation
Miclat, J. (2018). Calcium Regulation of a Slow AHP in Hippocampal Pyramidal Cells (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/31781