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Activation of the CA2-ventral CA1 pathway reverses social discrimination dysfunction in Shank3B knockout mice.
Cope, Elise C; Wang, Samantha H; Waters, Renée C; Gore, Isha R; Vasquez, Betsy; Laham, Blake J; Gould, Elizabeth.
Affiliation
  • Cope EC; Princeton Neuroscience Institute, Princeton University, Princeton, NJ, 08544, USA.
  • Wang SH; Department of Neuroscience, University of Virginia School of Medicine, Charlottesville, VA, 22908, USA.
  • Waters RC; Princeton Neuroscience Institute, Princeton University, Princeton, NJ, 08544, USA.
  • Gore IR; Princeton Neuroscience Institute, Princeton University, Princeton, NJ, 08544, USA.
  • Vasquez B; Princeton Neuroscience Institute, Princeton University, Princeton, NJ, 08544, USA.
  • Laham BJ; Princeton Neuroscience Institute, Princeton University, Princeton, NJ, 08544, USA.
  • Gould E; Princeton Neuroscience Institute, Princeton University, Princeton, NJ, 08544, USA.
Nat Commun ; 14(1): 1750, 2023 03 29.
Article in En | MEDLINE | ID: mdl-36991001
Mutation or deletion of the SHANK3 gene, which encodes a synaptic scaffolding protein, is linked to autism spectrum disorder and Phelan-McDermid syndrome, conditions associated with social memory impairments. Shank3B knockout mice also exhibit social memory deficits. The CA2 region of the hippocampus integrates numerous inputs and sends a major output to the ventral CA1 (vCA1). Despite finding few differences in excitatory afferents to the CA2 in Shank3B knockout mice, we found that activation of CA2 neurons as well as the CA2-vCA1 pathway restored social recognition function to wildtype levels. vCA1 neuronal oscillations have been linked to social memory, but we observed no differences in these measures between wildtype and Shank3B knockout mice. However, activation of the CA2 enhanced vCA1 theta power in Shank3B knockout mice, concurrent with behavioral improvements. These findings suggest that stimulating adult circuitry in a mouse model with neurodevelopmental impairments can invoke latent social memory function.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Autism Spectrum Disorder Type of study: Prognostic_studies Limits: Animals Language: En Journal: Nat Commun Journal subject: BIOLOGIA / CIENCIA Year: 2023 Document type: Article Affiliation country: United States Country of publication: United kingdom

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Autism Spectrum Disorder Type of study: Prognostic_studies Limits: Animals Language: En Journal: Nat Commun Journal subject: BIOLOGIA / CIENCIA Year: 2023 Document type: Article Affiliation country: United States Country of publication: United kingdom