The Na⁺-activated K⁺ channel Slack contributes to synaptic development and plasticity.

ABSTRACT: Human mutations of the Na⁺-activated K⁺ channel Slack (KCNT1) are associated with epilepsy and intellectual disability. Accordingly, Slack knockout mice (Slack^-/-) exhibit cognitive flexibility deficits in distinct behavioral tasks. So far, however, the underlying causes as well as the role of Slack in hippocampus-dependent memory functions remain enigmatic. We now report that infant (P6-P14) Slack^-/- lack both hippocampal LTD and LTP, likely due to impaired NMDA receptor (NMDAR) signaling. Postsynaptic GluN2B levels are reduced in infant Slack^-/-, evidenced by lower amplitudes of NMDAR-meditated excitatory postsynaptic potentials. Low GluN2B affected NMDAR-mediated Ca²⁺-influx, rendering cultured hippocampal Slack^-/-</

SUBMITTER: Matt L 

PROVIDER: S-EPMC8629810 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature