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<p>Atp8a2 is a type of phospholipid flippases, highly expressed in the cerebellum, functioning to maintain the stability and normal function of the cytomembrane by transporting phosphatidylserine into the cytoplasmic membrane. Atp8a2 mutations and knockout can cause neuronal PS externalization and cerebellar ataxia. The cerebellar damage caused by acrylamide (ACR) exposure has similar pathological features to the symptoms caused by Atp8a2 mutations and knockout. However, the expression of Atp8a2 in the cerebellum and whether Atp8a2 alterations are involved in the pathogenesis of ACR neurotoxicity remain unclear. Here, we find that gavage of 0.5&#xa0;mg/kg and higher doses of ACR decreased Atp8a2 expression in male SD rats’ Purkinje cells, while the loss of Purkinje cells was observed only at 20&#xa0;mg/kg. The upregulation of Atp8a2 blocks phosphatidylserine externalization and the loss of Purkinje cells and mitigates the increase in the number of microglia in SD rats exposed to 20&#xa0;mg/kg ACR. These suggest that Atp8a2 expression is sensitive to the neurotoxicity of ACR, and decreased Atp8a2 expression is involved in the mechanism of ACR-induced cerebellar injury. This study provides a new important clue for understanding the mechanism of ACR-induced cerebellar lesions and evaluating dose standards for ACR neurotoxicity.</p>

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A decrease in Atp8a2 expression in Purkinje cells mediated acrylamide-induced cerebellar pathology in rats

  • 期刊论文

  • 发表日期：

    2025年10月14日

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  • Kai Yan,
  • Wenhui Liu,
  • Siqi Xu,
  • Lifang Li,
  • Jiaqi Zhang,
  • Zhoutong Luo,
  • Guoying Li,
  • Junhua Yang

摘要

Atp8a2 is a type of phospholipid flippases, highly expressed in the cerebellum, functioning to maintain the stability and normal function of the cytomembrane by transporting phosphatidylserine into the cytoplasmic membrane. Atp8a2 mutations and knockout can cause neuronal PS externalization and cerebellar ataxia. The cerebellar damage caused by acrylamide (ACR) exposure has similar pathological features to the symptoms caused by Atp8a2 mutations and knockout. However, the expression of Atp8a2 in the cerebellum and whether Atp8a2 alterations are involved in the pathogenesis of ACR neurotoxicity remain unclear. Here, we find that gavage of 0.5 mg/kg and higher doses of ACR decreased Atp8a2 expression in male SD rats’ Purkinje cells, while the loss of Purkinje cells was observed only at 20 mg/kg. The upregulation of Atp8a2 blocks phosphatidylserine externalization and the loss of Purkinje cells and mitigates the increase in the number of microglia in SD rats exposed to 20 mg/kg ACR. These suggest that Atp8a2 expression is sensitive to the neurotoxicity of ACR, and decreased Atp8a2 expression is involved in the mechanism of ACR-induced cerebellar injury. This study provides a new important clue for understanding the mechanism of ACR-induced cerebellar lesions and evaluating dose standards for ACR neurotoxicity.