Prenatal exposure to valproic acid reduces synaptic δ-catenin levels and disrupts ultrasonic vocalization in neonates.
Seung Hyun RohHadassah Mendez-VazquezMatheus F SathlerMichael J DoolittleAnastasiya ZaytsevaHannah BrownMorgan SainsburySeonil KimPublished in: bioRxiv : the preprint server for biology (2023)
Prenatal exposure of valproic acid (VPA) in mice significantly reduces synaptic δ-catenin protein and AMPA receptor levels in the pups' brains.VPA treatment significantly impairs dendritic branching in cultured cortical neurons, which is reversed by increased δ-catenin expression.VPA exposed pups exhibit impaired communication such as ultrasonic vocalization.Neuronal activation linked to ultrasonic vocalization is absent in VPA-exposed pups.The loss of δ-catenin functions underlies VPA-induced autism spectrum disorder (ASD) in early childhood.
Keyphrases
- autism spectrum disorder
- epithelial mesenchymal transition
- cell proliferation
- pregnant women
- attention deficit hyperactivity disorder
- poor prognosis
- intellectual disability
- high glucose
- endothelial cells
- diabetic rats
- oxidative stress
- skeletal muscle
- signaling pathway
- long non coding rna
- drug induced
- amino acid
- insulin resistance