This study assesses the hypothesis that severe thiamine deficiency may lead to a depletion of cerebral ACh, which, in turn, may be responsible for the cerebral dysfunction seen in this condition. Acetylcholine assays were carried out in rats with diet-induced thiamine deficiency resulting in overt neurologic signs and in asymptomatic pair-fed and normally fed controls. The brainstem and cerebellum were assayed, in addition to the cortex, since the former sites exhibit the most significant biochemical alterations in thiamine deficiency. Acetylcholine was assayed by a modification of a specific and accurate fluorometric procedure. For every brain area studied the cerebral ACh concentrations in thiamine-deficient rats exhibiting overt neurologic signs were comparable to values seen in asymptomatic pair-fed controls. This study indicates that thiamine deficiency does not cause an alteration in cerebral regional ACh stores and that alternate mechanisms for the neurologic dysfunction will have to be sought.
|Original language||English (US)|
|Number of pages||5|
|Journal||Proceedings of the Society for Experimental Biology and Medicine|
|Publication status||Published - Sep 1970|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)