The Overexpression of eIF4E Decreases Oxytocin Levels and Induces Social Cognitive Behavioral Disorders in Mice.

Abstract

Overexpression of the eukaryotic initiation factor 4E (eIF4E) gene has been associated with excessive stereotypic behaviors and reduced sociability, which manifest as autism-like social cognitive deficits. However, the precise mechanisms by which eIF4E overexpression insufficiently induces these autism-like behaviors and the specific brain regions implicated remain insufficiently understood. Oxytocin (OXT), a neurotransmitter known for its role in social behavior, has been proposed to modulate certain autism-related symptoms by influencing microglial function and attenuating neuroinflammation. Nonetheless, the contributions of the hippocampus and oxytocin in the content of eIF4E overexpression-induced autistic behaviors remain elucidated. To investigate this issue, researchers utilized the three-chamber social interaction test, the open-field test, and the Morris water maze to evaluate the social cognitive behaviors of the two groups of mice. Additionally, ELISA, immunofluorescence, Western blotting, and qRT-PCR were employed to quantify oxytocin levels and assess hippocampal microglial activation. The results indicate that overexpression of eIF4E in mice is associated with significant impairments in social cognition, alongside pronounced marked hyperactivation of hippocampal microglia.