Lucas Matt, Thomas Pham, David Skrabak, Felix Hoffmann, Philipp Eckert, Jiaqi Yin, Miriam Gisevius, Rebekka Ehinger, Anne Bausch, Marius Ueffing, Karsten Boldt, Peter Ruth, Robert Lukowski
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...
December 2021: Cellular and Molecular Life Sciences: CMLS