title: Reduced K+ channel inactivation, spike broadening, and after-hyperpolarization in Kvbeta1.1-deficient mice with impaired learning.
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.
authors.affiliation: Cold Spring Harbor Laboratory, New York 11724, USA.
authors.forename: K P
authors.initials: KP
authors.lastname: Giese
authors.forename: J F
authors.initials: JF
authors.lastname: Storm
authors.forename: D
authors.initials: D
authors.lastname: Reuter
authors.forename: N B
authors.initials: NB
authors.lastname: Fedorov
authors.forename: L R
authors.initials: LR
authors.lastname: Shao
authors.forename: T
authors.initials: T
authors.lastname: Leicher
authors.forename: O
authors.initials: O
authors.lastname: Pongs
authors.forename: A J
authors.initials: AJ
authors.lastname: Silva
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000502:physiology; D003463:Cues; D005071:Evoked Potentials / Q000502:physiology*; D005518:Food Preferences; D006624:Hippocampus / Q000473:pathology / Q000502:physiology* / Q000503:physiopathology; D051662:Kv1.1 Potassium Channel; D051664:Kv1.3 Potassium Channel; D051038:Large-Conductance Calcium-Activated Potassium Channel beta Subunits; D007859:Learning Disabilities / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D018782:Maze Learning / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout; D009473:Neuronal Plasticity; D015221:Potassium Channels / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D024642:Potassium Channels, Voltage-Gated; D017966:Pyramidal Cells / Q000473:pathology / Q000502:physiology*; D012919:Social Behavior; D013569:Synapses / Q000502:physiology
chemical_list: C496947:Kcna1 protein, mouse; C494838:Kcnab1 protein, mouse; D051664:Kv1.3 Potassium Channel; D051038:Large-Conductance Calcium-Activated Potassium Channel beta Subunits; D015221:Potassium Channels; D024642:Potassium Channels, Voltage-Gated; D051662:Kv1.1 Potassium Channel; D002118:Calcium