Early studies showed that the development of neurological abnormalities in thiamin deficiency did not follow the same time course as the impairment of pyruvate and 2-oxoglutarate dehydrogenase or transketolase activities. The brain regions in which metabolic disturbances are most marked were not those that are vulnerable to anatomical lesions. These studies suggested a function for thiamin in the nervous system other than its coenzyme role.
Thiamin triphosphate is formed in brain and skeletal muscle by phospho-rylation of thiamin diphosphate (Section 6.2), and its concentration is very precisely controlled, because there is also an active thiamin triphosphatase (Lakaye et al., 2002). In nervous tissue thiamin triphosphate is localized
more-or-less completely in the membrane fraction, whereas in muscle it is mainly cytosolic.
Early studies showed that thiamin triphosphate had a role in electrical conduction in nerve cells; more recent studies have shown that it activates a chloride channel in the nerve membrane, acting as a phosphate donor (Bettendorff etal., 1994; Bettendorff, 1996). It also acts as a phosphate donor to othermem-brane proteins in nerve and synaptosome preparations (Nghiem et al., 2000).
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