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

Kai Yan¹, Wenhui Liu¹, Siqi Xu¹

¹Department of Anatomy, School of Basic Medical Sciences, Guangdong Pharmaceutical University, Room 514#, Building of Basic Medical Science, No. 280, East Waihuan Street, Higher Education Mega Center, Guangzhou City, 510006 Guangdong Province China.

Toxicological Research

|March 2, 2026

Summary

This summary is machine-generated.

Acrylamide (ACR) exposure reduces Atp8a2 expression in rat cerebellum, contributing to neurotoxicity. Upregulating Atp8a2 can protect against ACR-induced cerebellar damage and cell loss.

Keywords:

Acrylamide Ataxia Neurotoxicity Phospholipid flippases

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Area of Science:

Neuroscience
Toxicology
Cell Biology

Background:

Atp8a2 is crucial for cerebellar membrane stability and function.
Atp8a2 mutations cause cerebellar ataxia, similar to acrylamide (ACR) exposure.
The role of Atp8a2 in ACR neurotoxicity is currently unknown.

Purpose of the Study:

To investigate Atp8a2 expression changes in the cerebellum following ACR exposure.
To determine if Atp8a2 alterations contribute to ACR-induced cerebellar injury.

Main Methods:

Male Sprague-Dawley rats were exposed to varying doses of ACR via gavage.
Atp8a2 expression levels in Purkinje cells were measured.
Neuronal loss, phosphatidylserine externalization, and microglial activation were assessed.

Main Results:

ACR exposure (≥0.5 mg/kg) decreased Atp8a2 expression in Purkinje cells.
Significant Purkinje cell loss occurred at 20 mg/kg ACR.
Atp8a2 upregulation mitigated ACR-induced cell loss, PS externalization, and microgliosis.

Conclusions:

Atp8a2 expression is sensitive to ACR neurotoxicity.
Reduced Atp8a2 expression is implicated in the mechanism of ACR-induced cerebellar damage.
This finding offers insights into ACR neurotoxicity mechanisms and dose evaluation.