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. 2023 Jan 10;14:1090865. doi: 10.3389/fnsyn.2022.1090865

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Copyright © 2023 Sabo, Lahr, Offer, Weekes and Sceniak.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Expression of a GluN2B variant reduces LTD. Mice were generated that were heterozygous for the disease-associated missense variant, C456Y, in the LBD (Shin et al., 2020). At postnatal day 19–23, field EPSPs (fEPSPs) were recorded from CA1 neurons in acute hippocampal slices. Neurons expressing the C456Y variant had impaired NMDAR-dependent LTD, induced by low frequency stimulation (LFS). Synapse density and postsynaptic ultrastructure were unaffected. Illustrations were partially created with BioRender.com. Recordings are from Shin et al. (2020).