Cerebral glucose metabolism in unilateral entorhinal cortex-lesioned rats: an animal PET study.
To evaluate the effect of entorhinal cortical lesion on cerebral cortical function, we studied cerebral glucose utilization (CMRGlc) using a high resolution PET scanner after quinolinic acid lesion of the unilateral entorhinal cortex in rats. [18F]Fluorodeoxyglucose PET was performed at 4 days and 4 weeks after surgery, and CMRGlc in the bilateral frontal, parietal and temporal regions were analyzed. At 4 days, the entorhinal lesion induced a 12-15% decrease in CMRGlc of frontal, parietal and temporal regions ipsilateral to the lesion. The hypometabolism continued at 4 weeks in the temporal region. These findings suggest that entorhinal lesion induces cerebral cortical hypometabolism, which implies a pathogenetic role of entorhinal area on the cortical hypometabolism in Alzheimer's disease.
Hayashi
T
T
Department of Neurology, Faculty of Medicine, Kyoto University, Japan.
Fukuyama
H
H
Katsumi
Y
Y
Hanakawa
T
T
Nagahama
Y
Y
Yamauchi
H
H
Tsukada
H
H
Shibasaki
H
H
D000704:Analysis of Variance; D000818:Animals; D018728:Entorhinal Cortex / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D008297:Male; D009498:Neurotoxins / Q000633:toxicity; D051381:Rats; D017208:Rats, Wistar; D014055:Tomography, Emission-Computed
D009498:Neurotoxins; D005947:Glucose