Quantitative and qualitative microbiota composition of the distal colon of rats in different terms of experimental 6-OHDA-induced parkinsonism (pilot study)

V. Stetska, N. Shystavetska, T. Serhiychuk, T. Dovbynchuk, G. Tolstanova
Taras Shevchenko National University of Kyiv, Kyiv; Taras Shevchenko National University of Kyiv, Kyiv; Taras Shevchenko National University of Kyiv, Kyiv; Taras Shevchenko National University of Kyiv, Kyiv; Taras Shevchenko National University of Kyiv, Kyiv

Abstract


In the aspect of the existence of the gut brain axis are considered quantitative changes of the distal part of colon's microbiota (Mb) under conditions of experimental parkinsonism. Studies were done on laboratory non-linear male rats (140–160 g, n = 7). Parkinsonism was modeled by onesided destruction of the dopaminergic neurons of a compact part of the substantia nigra of brain, causing by stereotaxic microinjections 12 mg neurotoxin 6-OHDA (Sigma-Aldrich, Germany) in the left lateral ascending bundle. Changes in the quantitative Mb composition were determined bacteriologically by sowing 10-fold dilutions of fecal biopsy on differential diagnostic media (HiMedia, India) in 1, 1.5, 2 months after induced parkinsonism. Research has been shown that within the fecal Mb of rats, within 2 months from the beginning of the experiment, significant changes were detected only for E.coli. The amount of lac(+) E.coli increased from 1,5 months to 2 folds (from lg 4,65 ± 0,80 CFU/g to lg 6,08 ± 0,70 CFU/g  (1,5 months), after 2 months – from lg 4.39±0.55 CFU/g to lg 6.24±1.26 CFU/g. At the same time, the amount of E.coli lac(-) decreased by 2-3 folds. The number of the genus Bifidobacterium and Lactobacillus remained within the control values. After 2 months after induced parkinsonism, there was a tendency to increase the number of Clostridium species. These results suggest minor microbiota changes of 6-OHDA-induced parkinsonism in rats. These results are preliminary and require more detailed study.

Keywords


microbiota, Parkinson's disease, neurodegeneration

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Received in the editorial: 15.08.2018

Received a revised version: 17.09.2018

Signed in the press: 17.09.2018


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