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

Frank R Sharp, E. Bolger, K. Evans

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

The effects of thiamine (B1) deficiency on local CMR(glu) (LMCR(glu)) 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: bilateral vestibular nuclei lesions in symptomatic animals; very low LCMR(glu) rates in these lesions; and limitation of glial proliferation in the lesions. Giving B1 to B1-deficient symptomatic animals produced a cellular proliferative response consisting mostly of microglia in the lesioned areas of the vestibular nuclei and a high LCMR(glu) rate in the regions of microglial proliferation.

Original languageEnglish (US)
Pages (from-to)203-207
Number of pages5
JournalJournal of Cerebral Blood Flow and Metabolism
Volume2
Issue number2
StatePublished - 1982

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Thiamine Deficiency
Vestibular Nuclei
Neuroglia
Glucose
Brain
Deoxyglucose
Microglia
Ataxia
Diet

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Neuroscience(all)

Cite this

Thiamine deficiency limits glucose utilization and glial proliferation in brain lesions of symptomatic rats. / Sharp, Frank R; Bolger, E.; Evans, K.

In: Journal of Cerebral Blood Flow and Metabolism, Vol. 2, No. 2, 1982, p. 203-207.

Research output: Contribution to journalArticle

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