REDUCED K-HYPERPOLARIZATION IN KV-BETA-1.1-DEFICIENT MICE WITH IMPAIRED LEARNING( CHANNEL INACTIVATION, SPIKE BROADENING, AND AFTER)

A-type K+ channels are known to regulate neuronal firing, but their ro le in repetitive firing and learning in mammals is not well. character ized. To determine the contribution of the auxiliary K+ channel subuni t Kv beta 1.1 to A-type K+ currents and to study the physiological rol e of A-type KC channels in repetitive firing and learning, we deleted the Kv beta 1.1 gene in mice. The loss of Kv beta 1.1 resulted in a re duced K+ current inactivation in hippocampal CAI pyramidal neurons. Fu rthermore, in the mutant neurons, frequency-dependent spike broadening and the slow afterhyperpolarization (sAHP) were reduced. This suggest s that Kv beta 1.1-dependent A-type K+ channels contribute to frequenc y-dependent spike broadening and may regulate the sAHP by controlling Ca2+ influx during action potentials. The Kv beta 1.1-deficient mice s howed normal synaptic plasticity but were impaired in the learning of a water maze test and in the social transmission of food preference ta sk, indicating that the Kv beta 1.1 subunit contributes to certain typ es of learning and memory.