Vitamin B6 Deficiency Induces Autism-Like Behaviors in Rats by Regulating mTOR-Mediated Autophagy in the Hippocampus

Figure 6

VB₆ deficiency suppressed generation of GABAergic interneurons and autophagy by activating mTOR pathway in hippocampus in offspring rats. The offspring rats obtained from their pregnant mothers with VB₆ deficiency was subjected to the modeling and were intraperitoneally injected with NVP-BEZ235 (400 μg/kg) or Clonazepam (0.025 mg/kg) 30 minutes before behavioral tests. Following drug administration, hippocampal tissues were collected after euthanasia of offspring. (a, b, c, and d) The levels of autophagy-related proteins (LC3 I, LC3 II, and p62) and mTOR pathway-related proteins (mTOR and p-mTOR) were measured by Western blot. GAPDH was used as the loading control. (e) The expression of GABA⁺ in the hippocampal CA3 area of offspring rats was determined using immunofluorescence staining (×100 magnification, scale bar: 50 μm). Three rats/group. One-way analysis of variance with Dunnett’s post-hoc test. VB₆: vitamin B6; GABA⁺: gamma-aminobutyric acid-positive; mTOR: mammalian target of rapamycin; p-mTOR: phosphor-mTOR; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; ^^^ vs. VB₆ deficiency.

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