Early postnatal dysfunction of ACC PV interneurons in Shank3B^-/- mice.

ABSTRACT: Anterior cingulate cortex (ACC) dysfunction is implicated in the cognitive and social deficits associated with autism spectrum disorder (ASD), yet the developmental trajectory of ACC circuit maturation in ASD remains poorly understood. Here, we examined the postnatal development of glutamatergic synaptic connectivity and intrinsic excitability in layer 2/3 pyramidal neurons (PYRs) and Parvalbumin-expressing interneurons (PVINs) in the ACC of mice harboring a deletion in SHANK3 (Shank3B^-/-), a well-established genetic cause of autism. We found that ACC PVINs in Shank3B^-/- mice exhibit reduced excitability and in vivo hypoactivity as early as postnatal day 15 (P15) despite receiving normal levels of glutamatergic input. Early PVIN hypoexcitability is associated with dec

SUBMITTER: Shih YC 

PROVIDER: S-EPMC12532719 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature