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Abstract Aims This study aims to elucidate how the hyperactivated enteric glial cells (EGCs) trigger Parkinson's Disease (PD) pathogenesis and if exogenous gut-brain regulatory hormone oxytocin could alleviate the phenotypes of PD. Methods Prodromal and clinical PD mice model were established via intragastric administration of rotenone (ROT). Intestinal and motor function of the mice were assessed. The expression of glial fibrillary acidic protein (GFAP), oxytocin receptor (OXTR) and tyrosine hydroxylase (TH) in the colon and midbrain were detected by immunofluorescence staining. The levels of α-synuclein (α-syn), oxytocin (OXT), and inflammatory factors in serum and colon were measured by ELISA, western blotting and qPCR. Exogenous OXT and EGCs inhibitor fluorocitrate (FC) were administered, and the rescue effect on PD mice was assessed by neurobehavioral assays. Results ROT administration induced constipation and motor PD symptoms in mice successively. The expression of GFAP and α-syn in the colon of PD mice were increased, while the OXT and OXTR levels were downregulate. Exogenous OXT or FC administration inhibited EGCs hyperactivation, reduced inflammatory factors levels and α-syn accumulation, and ultimately alleviated prodromal and clinical PD phenotypes. Conclusions EGCs hyperactivation plays a crucial role in PD pathogenesis, and exogenous OXT or FC could ameliorate the prodromal and clinical PD phenotypes.
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