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• W2109403460 abstract "A-type K+ channels are known to regulate neuronal firing, but their role in repetitive firing and learning in mammals is not well characterized. To determine the contribution of the auxiliary K+ channel subunit Kvbeta1.1 to A-type K+ currents and to study the physiological role of A-type K+ channels in repetitive firing and learning, we deleted the Kvbeta1.1 gene in mice. The loss of Kvbeta1.1 resulted in a reduced K+ current inactivation in hippocampal CA1 pyramidal neurons. Furthermore, in the mutant neurons, frequency-dependent spike broadening and the slow afterhyperpolarization (sAHP) were reduced. This suggests that Kvbeta1.1-dependent A-type K+ channels contribute to frequency-dependent spike broadening and may regulate the sAHP by controlling Ca2+ influx during action potentials. The Kvbeta1.1-deficient mice showed normal synaptic plasticity but were impaired in the learning of a water maze test and in the social transmission of food preference task, indicating that the Kvbeta1.1 subunit contributes to certain types of learning and memory." @default.
• W2109403460 created "2016-06-24" @default.
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• W2109403460 date "1998-09-01" @default.
• W2109403460 modified "2023-10-17" @default.
• W2109403460 title "Reduced K⁺ Channel Inactivation, Spike Broadening, and After-Hyperpolarization in Kvβ1.1-Deficient Mice with Impaired Learning" @default.
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• W2109403460 doi "https://doi.org/10.1101/lm.5.4.257" @default.
• W2109403460 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/311244" @default.
• W2109403460 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10454353" @default.
• W2109403460 hasPublicationYear "1998" @default.
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