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The streptozotocin-induced rat model of diabetes mellitus evidences significant reduction of myosin-Va expression in the brain

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Abstract

Diabetes mellitus is a disease characterized by increased glucose levels in the blood. Hyperglycemia causes damage to the brain tissue, and induces significant changes in synaptic transmission. In this investigation, we have found a significant alteration in the expression of the molecular motor involved in the synaptic vesicles transport, myosin-Va, and its distribution in rat brains of streptozotocin-induced diabetes model. Brains were removed after 20 days, homogenized and analysed by Western blotting, qRT-PCR and immunohistochemistry. Myosin-Va presented significantly lower levels of both mRNA and protein in diabetic than those observed in non-diabetic animals. Moreover, neuronal and glial cells of the occipital and frontal cortex exhibited decreased myosin-Va immunostaining in diabetic rat brains. In conclusion, diabetic rat brains displayed altered expression and distribution of myosin-Va, and these finding may contribute to the basic understanding about this myosin role in brain function related to diabetes.

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Acknowledgments

This work was supported by grants from FAPEMIG to FSE, from CNPq to LRG, by ProBiotec fellowship to AVC, by CAPES fellowship to LKC and RN. We thank Ms. Neire Moura de Gouveia, Fabiana Barcelos Furtado and Fernanda Vieira Alves (INGEB-UFU) for contributions to experimental procedures. We also express our gratitude to the Professor Dr. Marcelo Emílio Beletti at ICBIM-UFU for taking time on many occasions to discuss our immunohistochemistry data with us.

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The authors are not having any conflict of interest related to this paper.

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Correspondence to Foued Salmen Espindola.

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da Costa, A.V., Calábria, L.K., Nascimento, R. et al. The streptozotocin-induced rat model of diabetes mellitus evidences significant reduction of myosin-Va expression in the brain. Metab Brain Dis 26, 247–251 (2011). https://doi.org/10.1007/s11011-011-9259-5

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  • DOI: https://doi.org/10.1007/s11011-011-9259-5

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