Effects of Exercise Training on the Phosphoproteomics of the Medial Prefrontal Cortex in Rats With Autism Spectrum Disorder Induced by Valproic Acid.

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  • Additional Information
    • Source:
      Publisher: Sage Publications Country of Publication: United States NLM ID: 100892086 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1552-6844 (Electronic) Linking ISSN: 15459683 NLM ISO Abbreviation: Neurorehabil Neural Repair Subsets: MEDLINE
    • Publication Information:
      Publication: 2002- : Thousand Oaks, CA : Sage Publications
      Original Publication: New York, NY : Demos Medical Pub., c1999-
    • Subject Terms:
      Valproic Acid*/adverse effects ; Autism Spectrum Disorder*/chemically induced; Rats ; Animals ; Phosphopeptides/adverse effects ; Prefrontal Cortex ; Behavior, Animal ; Disease Models, Animal
    • Abstract:
      Background: The key neural pathological characteristics of autism spectrum disorder (ASD) include abnormal synaptic plasticity of the medial prefrontal cortex (mPFC). Exercise therapy is widely used to rehabilitate children with ASD, but its neurobiological mechanism is unclear.
      Methods: To clarify whether the structural and molecular plasticity of synapses in the mPFC are related to improvement in ASD behavioral deficits after continuous exercise rehabilitation training, we applied phosphoproteomic, behavioral, morphological, and molecular biological methods to investigate the impact of exercise on the phosphoprotein expression profile and synaptic structure of the mPFC in valproic acid (VPA)-induced ASD rats.
      Results: Exercise training differentially regulated the density, morphology, and ultrastructure of synapses in mPFC subregions in the VPA-induced ASD rats. In total, 1031 phosphopeptides were upregulated and 782 phosphopeptides were downregulated in the mPFC in the ASD group. After exercise training, 323 phosphopeptides were upregulated, and 1098 phosphopeptides were downregulated in the ASDE group. Interestingly, 101 upregulated and 33 downregulated phosphoproteins in the ASD group were reversed after exercise training, and these phosphoproteins were mostly involved in synapses. Consistent with the phosphoproteomics data, the total and phosphorylated levels of the proteins MARK1 and MYH10 were upregulated in the ASD group and reversed after exercise training.
      Conclusions: The differential structural plasticity of synapses in mPFC subregions may be the basic neural architecture of ASD behavioral abnormalities. The phosphoproteins involved in mPFC synapses, such as MARK1 and MYH10, may play important roles in the exercise rehabilitation effect on ASD-induced behavioral deficits and synaptic structural plasticity, which requires further investigation.
    • Contributed Indexing:
      Keywords: autism spectrum disorder; exercise training; medial prefrontal cortex; phosphoproteomics; synaptic structure
    • Accession Number:
      614OI1Z5WI (Valproic Acid)
      0 (Phosphopeptides)
    • Publication Date:
      Date Created: 20230302 Date Completed: 20230407 Latest Revision: 20230413
    • Publication Date:
      20240829
    • Accession Number:
      10.1177/15459683231152814
    • Accession Number:
      36860155