Expression of NMDA receptor and microRNA-219 in rats submitted to cerebral ischemia associated with alcoholism

ABSTRACT Alcohol consumption aggravates injuries caused by ischemia. Many molecular mechanisms are involved in the pathophysiology of cerebral ischemia, including neurotransmitter expression, which is regulated by microRNAs. Objective: To evaluate the microRNA-219 and NMDA expression in brain tissue...

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Published in:Arquivos de neuro-psiquiatria Vol. 75; no. 1; pp. 30 - 35
Main Authors: Silva, Cristiane Iozzi, Novais, Paulo Cézar, Rodrigues, Andressa Romualdo, Carvalho, Camila A.M., Colli, Benedicto Oscar, Carlotti, Carlos Gilberto, Tirapelli, Luís Fernando, Tirapelli, Daniela P.C.
Format: Journal Article
Language:English
Published: Rua do Matoso 170, Rio de Janeiro, RJ, CEP 20270-135, Brazil Thieme Revinter Publicações Ltda 01-01-2017
Academia Brasileira de Neurologia - ABNEURO
Academia Brasileira de Neurologia (ABNEURO)
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Summary:ABSTRACT Alcohol consumption aggravates injuries caused by ischemia. Many molecular mechanisms are involved in the pathophysiology of cerebral ischemia, including neurotransmitter expression, which is regulated by microRNAs. Objective: To evaluate the microRNA-219 and NMDA expression in brain tissue and blood of animals subjected to cerebral ischemia associated with alcoholism. Methods: Fifty Wistar rats were divided into groups: control, sham, ischemic, alcoholic, and ischemic plus alcoholic. The expression of microRNA-219 and NMDA were analyzed by real-time PCR. Results: When compared to the control group, the microRNA-219 in brain tissue was less expressed in the ischemic, alcoholic, and ischemic plus alcoholic groups. In the blood, this microRNA had lower expression in alcoholic and ischemic plus alcoholic groups. In the brain tissue the NMDA gene expression was greater in the ischemic, alcoholic, and ischemic plus alcoholic groups. Conclusion: A possible modulation of NMDA by microRNA-219 was observed with an inverse correlation between them.
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ISSN:0004-282X
1678-4227
1678-4227
0004-282X
DOI:10.1590/0004-282X20160188