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Acta Physiologica 2007; Volume 190, Supplement 656
The Scandinavian Physiological Society's Annual Meeting
8/10/2007-8/12/2007
Oslo, Norway
FUNCTIONS OF POSTSYNAPTIC ION CHANNELS IN HIPPOCAMPAL PYRAMIDAL NEURONS
Abstract number: 0204
Storm1 JF
1Institute of Physiology, IMB and Centre for Molecular Biology and Neuroscience, University of Oslo, 0317 Oslo, Norway
Although only two ionic currents are needed to generate action potentials, the postsynaptic compartments of neurons are typically equipped with tens of ion channel types. Many of these operate primarily in the sub-threshold voltage range, generating currents at membrane potentials negative to the spike threshold. Although these sub-threshold currents are often small, they play pivotal roles in determining WHETHER, WHEN and HOW OFTEN action potentials occur, thus shaping postsynaptic neural coding and information processing. Here we focus on sub-threshold ion channels in CA1 pyramidal neurons a cell type involved in learning and memory, and in brain disorders like epilepsy, brain ischemia, and dementia. Using results from somatic and dendritic recordings, dynamic clamp, and computational modelling, I will discuss: (1) Channels that regulate excitability and spike timing in response to excitatory synaptic input, temporal integration, and the threshold for long-term synaptic plasticity. (2) Sub-threshold resonance at theta ([theta]) frequencies (58 Hz), contributing to network [theta] oscillations during spatial exploration and learning. Combining whole-cell recordings and computational modelling we describe mechanisms underlying two forms of [theta] resonance: M- and H-type (Hu et al. J Physiol 2002). Next, we showed that transgenic mice with less M-channels lacked M-resonance and were impaired in spatial learning (Peters et al. Nat Neurosci 2005). (3) Mechanisms and functions of feedback regulation of excitability in CA1 hippocampal pyramidal cells, including the roles of voltage- and Ca-activated channels in AHPs, ADPs, adaptation and bursting. (4) Novel roles of the persistent Na+ current and BK channels in regulation of excitability (Vervaeke et al. Neuron 2006; Gu et al. J Physiol 2007).
To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 190, Supplement 656 :0204