Key result
Intermediate-conductance Ca2+-dependent K+ (IKCa) channels underlie the slow afterhyperpolarization generated by synaptic input or postsynaptic stimuli in CA1 hippocampal pyramidal cells.
Identifies IKCa channels as the molecular basis for the slow afterhyperpolarization in central neurons, providing a potential target for pharmacological modulation.
Control over the frequency and pattern of neuronal spike discharge depends on Ca2+-gated K+ channels that reduce cell excitability by hyperpolarizing the membrane potential. The Ca2+-dependent slow afterhyperpolarization (sAHP) is one of the most prominent inhibitory responses in the brain, with sAHP amplitude linked to a host of circuit and behavioral functions, yet the channel that underlies the sAHP has defied identification for decades. Here, we show that intermediate-conductance Ca2+-dependent K+ (IKCa) channels underlie the sAHP generated by trains of synaptic input or postsynaptic stimuli in CA1 hippocampal pyramidal cells. These findings are significant in providing a molecular identity for the sAHP of central neurons that will identify pharmacological tools capable of potentially modifying the several behavioral or disease states associated with the sAHP.
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King et al. (2015) studied this question. IKCa channels was evaluated on slow afterhyperpolarization (sAHP). Intermediate-conductance Ca2+-dependent K+ (IKCa) channels underlie the slow afterhyperpolarization generated by synaptic input or postsynaptic stimuli in CA1 hippocampal pyramidal cells.
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