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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Thiamine deficiency limits glucose utilization and glial proliferation in brain lesions of symptomatic rats.

The effects of thiamine (B1) deficiency on local CMRglu (LMCRglu) in the vestibular nuclei were studied with the 14C-2-deoxyglucose autoradiographic method in awake asymptomatic and symptomatic rats. Animals on the B1-deficient diet for 98 days developed symptoms of ataxia and opisthotonos. The results show that B1 deficiency produces: (1) bilateral vestibular nuclei lesions in symptomatic animals; (2) very low LCMRglu rates in these lesions; and (3) limitation of glial proliferation in the lesions. Giving B1 to B1-deficient symptomatic animals produced a cellular proliferation response consisting mostly of microglia in the lesioned areas of the vestibular nuclei and a high LCMRglu rate in the regions of microglial proliferation.[1]

References

  1. Thiamine deficiency limits glucose utilization and glial proliferation in brain lesions of symptomatic rats. Sharp, F.R., Bolger, E., Evans, K. J. Cereb. Blood Flow Metab. (1982) [Pubmed]
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