ArticleNature communications2024
Conditional knockout of Shank3 in the ventral CA1 by quantitative in vivo genome-editing impairs social memory in mice.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Developmental CA2 perineuronal net reduction restores social memory in Shank3 mutant mice.Communications biology · 2026Article
- Maintaining and regaining episodic memory in Alzheimer disease: a circuit-based perspective.Nature reviews. Neurology · 2026Review
- Environmental context modulates sociability in ube3a zebrafish mutants via alterations in sensory pathways.Molecular psychiatry · 2026Article
- Distinct neural dynamics in the ventral hippocampus and medial prefrontal cortex during social information processing.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Heightened empathic responses led by imbalanced cortico-amygdala circuit inbioRxiv : the preprint server for biology · 2025Article
- Deficiency of Shank3 in the nucleus accumbens reveals a loss of social-specific motivation.Communications biology · 2025Article
- Developmental CA2 perineuronal net reduction restores social memory inbioRxiv : the preprint server for biology · 2025Article
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Abstract
Individuals with autism spectrum disorder (ASD) have a higher prevalence of social memory impairment. A series of our previous studies revealed that hippocampal ventral CA1 (vCA1) neurons possess social memory engram and that the neurophysiological representation of social memory in the vCA1 neurons is disrupted in ASD-associated Shank3 knockout mice. However, whether the dysfunction of Shank3 in vCA1 causes the social memory impairment observed in ASD remains unclear. In this study, we found that vCA1-specific Shank3 conditional knockout (cKO) by the adeno-associated virus (AAV)- or specialized extracellular vesicle (EV)- mediated in vivo gene editing was sufficient to recapitulate the social memory impairment in male mice. Furthermore, the utilization of EV-mediated Shank3-cKO allowed us to quantitatively examine the role of Shank3 in social memory. Our results suggested that there is a certain threshold for the proportion of Shank3-cKO neurons required for social memory disruption. Thus, our study provides insight into the population coding of social memory in vCA1, as well as the pathological mechanisms underlying social memory impairment in ASD.
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