Vitamin B6 (VB₆) exhibits therapeutic effects towards autism spectrum disorder (ASD), but its specific mechanism is poorly understood. Rat dams were treated with VB₆ standard, VB₆ deficiency, or VB₆ supplementary diet, and the same treatment was provided to their offspring, with their body weights monitored. Three-chambered social test and open field test were employed to evaluate the effect of VB₆ on autism-like behaviors. Gamma-aminobutyric acid (GABA) generation and synaptic inhibition of neurons in the hippocampus of rat were detected via immunofluorescence staining, followed by the measurement of GABA concentration through high-performance liquid chromatography (HPLC). The role of VB₆ in the autophagy and apoptosis of cells was determined via Western blot and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). In order to conduct rescue experiments, the inhibition of mammalian target of rapamycin (mTOR) or the activation of GABA was achieved by drug administration to the offspring rats with VB₆ deficiency. As a result, no evident difference in weight was observed in the offspring with varied VB₆ treatments. VB₆ deficiency impaired social interaction; aggravated self-grooming and bowel frequency; decreased GABA concentration, VIAAT, GAD67, vGAT expressions, and LC3 II/LC3 I ratio; increased p62 level and p-mTOR/mTOR ratio; and promoted cell apoptosis. Inhibition of mTOR reversed the effect of VB₆ deficiency on cell autophagy. GABA activation or mTOR inhibition offset the role of VB₆ deficiency in autism-like behaviors and hippocampal GABA expression. Collectively, VB₆ deficiency induces autism-like behaviors in rats by regulating mTOR-mediated autophagy in the hippocampus.

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