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- W4387332701 endingPage "3101.e5" @default.
- W4387332701 startingPage "3084" @default.
- W4387332701 abstract "Heterozygous mutations in the dual-specificity tyrosine phosphorylation-regulated kinase 1a (Dyrk1a) gene define a syndromic form of autism spectrum disorder. The synaptic and circuit mechanisms mediating DYRK1A functions in social cognition are unclear. Here, we identify a social experience-sensitive mechanism in hippocampal mossy fiber-parvalbumin interneuron (PV IN) synapses by which DYRK1A recruits feedforward inhibition of CA3 and CA2 to promote social recognition. We employ genetic epistasis logic to identify a cytoskeletal protein, ABLIM3, as a synaptic substrate of DYRK1A. We demonstrate that Ablim3 downregulation in dentate granule cells of adult heterozygous Dyrk1a mice is sufficient to restore PV IN-mediated inhibition of CA3 and CA2 and social recognition. Acute chemogenetic activation of PV INs in CA3/CA2 of adult heterozygous Dyrk1a mice also rescued social recognition. Together, these findings illustrate how targeting DYRK1A synaptic and circuit substrates as enhancers of DYRK1A function harbors the potential to reverse Dyrk1a haploinsufficiency-associated circuit and cognition impairments." @default.
- W4387332701 created "2023-10-05" @default.
- W4387332701 creator A5000618559 @default.
- W4387332701 creator A5005748248 @default.
- W4387332701 creator A5013589294 @default.
- W4387332701 date "2023-10-01" @default.
- W4387332701 modified "2023-10-18" @default.
- W4387332701 title "An inhibitory circuit-based enhancer of DYRK1A function reverses Dyrk1a-associated impairment in social recognition" @default.
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