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Effects of prior taurine administration in neuroprotection and prevention of the effects of chronic ethanol consumption in hippocampal neurogenesis

Grant number: 16/16982-5
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): November 01, 2016
Effective date (End): July 31, 2017
Field of knowledge:Health Sciences - Collective Health - Public Health
Principal researcher:Luiz Fernando Takase
Grantee:Victor Augusto Mattiuzzo
Home Institution: Centro de Ciências Biológicas e da Saúde (CCBS). Universidade Federal de São Carlos (UFSCAR). São Carlos , SP, Brazil

Abstract

Abusive and chronic consumption of ethanol is one of the major risk factors to health. It´s accounting for 4% of all diseases in the world. There is evidence that excessive consumption of ethanol cause permanent neurological damage in animals and humans, leading to the decline of cognitive functions such as learning and memory. These problems can be directly related neurodegeneration and inhibition of hippocampal neurogenesis. It is believed that the stimulation of hippocampal neurogenesis by administration of neuroactive substances, such as taurine, can prevent or at least minimize these severe cognitive and behavioral deficits commonly observed in alcoholic individuals. Taurine is a non-essential amino acid from one of the most abundant in the body, found in higher concentrations especially in structures whose tissues are more excitable. In the central nervous system (CNS), taurine has various functions, most related to neuroprotection and stimulation of neurogenesis. The present study aimed to analyze the effects of taurine administration in neuroprotection and prevention of ethanol-induced inhibition of hippocampal neurogenesis. Will be used Wistar rats, 2 months old, kept in animal facilities with controlled conditions of light and temperature. The animals receive daily injections of taurine (i.p., 300 mg / kg in sterile 0.9% saline, the volume of 2ml / kg) during the period of 28 days. The control group will receive only injection of the vehicle (saline 0.9%) during the same period. After this period, the animals are exposed to model forced consumption of ethanol, which had continuous access to a bottle containing only aqueous ethanol solution, without option of pure water, during the period of 28 days. The control group collects the bottles containing pure water. The animals will be submitted to the subject of omission test and then perfused. The brains are removed, post-fixed, cryoprotected and cut in coronal 40¼m section. The material will be processed with immunohistochemistry techniques against Ki-67 (proliferation) and DCX (neurogenesis). Another series is stained with cresyl violet for volumetric analysis of the hippocampus and quantifying the number of cells pictotic (apoptosis). This work may have interesting clinical correlations, since results can open new perspectives for the prevention of the effects of ethanol in the CNS. (AU)

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