Thiamine Deficiency Increases Ca2+ Current and Ca(V)1.2 L-type Ca2+ Channel Levels in Cerebellum Granular Neurons

Author(s)

Moreira-Lobo, Daniel C. ; Cruz, Jader S. ; Silva, Flavia R. ; Ribeiro, Fabiola M. ; Kushmerick, Christopher ; Oliveira, Fernando A.

• Document type: Journal article
• Source: Cellular and Molecular Neurobiology; v. 37, n. 3, p. 453-460, APR 2017.
• Web of Science Citations: 2

Abstract

Thiamine (vitamin B1) is co-factor for three pivotal enzymes for glycolytic metabolism: pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase. Thiamine deficiency leads to neurodegeneration of several brain regions, especially the cerebellum. In addition, several neurodegenerative diseases are associated with impairments of glycolytic metabolism, including Alzheimer's disease. Therefore, understanding the link between dysfunction of the glycolytic pathway and neuronal death will be an important step to comprehend the mechanism and progression of neuronal degeneration as well as the development of new treatment for neurodegenerative states. Here, using an in vitro model to study the effects of thiamine deficiency on cerebellum granule neurons, we show an increase in Ca2+ current density and Ca(V)1.2 expression. These results indicate a link between alterations in glycolytic metabolism and changes to Ca2+ dynamics, two factors that have been implicated in neurodegeneration. (AU)

• FAPESP's process: 12/50336-2 - Interaction among hypometabolism, calcium dynamics and neuronal excitability: implications in the degenerative process of Alzheimer's Disease
• Grantee: Fernando Augusto de Oliveira Ribeiro
• Support Opportunities: Research Grants - Young Investigators Grants