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Department of Neurosciences, University of California at San Diego, La Jolla, CA.
Local cerebral glucose utilization (LCGU) was measured in asymptomatic rats on a thiamine (B1)-dencient diet for 70 days and in symptomatic fats on a B1-deficient diet for 98 days. LCGU increased in postcommissural fornix (F), pyramidal tracts (P), and inferior internal capsule (CAI) of symptomatic, compared with asymptomatic B1-deficient rats but decreased in thalamic nuclei, auditory structures, and lesioned vestibular nuclei. B1administration to symptomatic rats improved symptoms; decreased LCGU in F, P, and CAI; increased LCGU in the lesioned vestibular nuclei; but decreased LCGU in mammillary nuclei, anteroventral nucleus of thalamus, and medial raphe. The results indicate that B1 deficiency symptoms correlate with LCGU changes in F and P and vestibular nuclei.
Address correspondence and reprint requests to: Dr. Sharp, Department of Neurosciences, Mail Code No. M024, UCSD School of Medicine, La Jolla, CA 92093.
This research was supported by NIMH Small Grant 1R03MH34257.
Accepted for publication January 19, 1982.
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