Mechanisms Responsible for the High Sensitivity of Neural Cells to Vitamin B Deficiency
Neurophysiology, ISSN: 1573-9007, Vol: 48, Issue: 6, Page: 429-448
2016
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Article Description
The available information on the mechanisms of involvement of vitamin B1 (thiamine) in vital processes in neural cells is analyzed. It is concluded that, together with the coenzymatic functions performed by this vitamin, the latter realizes “noncoenzymatic” functions. These functions play significant roles in cellular processes in various cells, and this is an indisputable fact. Some features of the structural/functional organization of neurons are responsible for the importance of thiamine-dependent processes for the maintenance of the functional activity of these cells. The accumulated data on the release of thiamine from neurons in the course of their excitation, as well as on the high dynamics of B metabolism in nerve cells related to rapid changes between states of excitation and inhibition, allow researchers to formulate an idea on the existence of a rapidly exchanged pool of thiamine ant its biologically active derivatives (“mobile thiamine pool”) in such cells. It is hypothesized that circulation of this pool between the main part of the intracellular space and presynaptic compartments of the synaptic structures is associated with changes in the membrane potential of nerve cells and modifications of cellular metabolism. This is confirmed by the data on coupling of the regulation of the mitochondrial multienzyme pyruvate dehydrogenase complex with the functioning of the excitable membranes. It is suggested that the interaction of thiamine with cytoskeletal proteins plays an important role in vitally important nonenzymatic processes realized by this vitamin in neural cells. The possible role of thiamine deficiency in the development of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and Wernicke’s encephalopathy, is discussed.
Bibliographic Details
Springer Science and Business Media LLC
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