ArticleCommunications biology2025
Social memory engram formation impairment in neuroligin-3 R451C knock-in mice is caused by disrupted prefrontal NMDA receptor-dependent potentiation.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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15 authors.
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Abstract
Autism spectrum disorders (ASDs) are characterized by profound social cognitive deficits, including impairments in social memory-the ability to recognize and remember familiar conspecifics. However, the mechanisms underlying these deficits remain poorly understood. Here, we identify a distinct population of medial prefrontal cortical neurons that encode individual conspecifics and form social memory engram cells (SMECs) through N-methyl-D-aspartate receptor (NMDAR)-dependent long-term potentiation (LTP). Using the Neuroligin 3 R451C knock-in mouse model of autism, we demonstrate that disrupted NMDAR-dependent LTP impairs the formation of SMECs, leading to social memory deficits. Notably, these deficits are rescued by a well-tolerated, once-weekly "pulsed" administration of D-cycloserine, a partial NMDAR agonist. Our findings underscore the pivotal role of NMDAR-dependent synaptic plasticity in social memory encoding and position NMDAR-targeted therapies as a compelling avenue for addressing social cognitive deficits in ASDs.
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