Decreased glucose utilization in discrete brain regions of rat in thioacetamide-induced hepatic encephalopathy as measured with [3H]-deoxyglucose.
To evaluate the possible contribution of bioenergetic failure in the particular brain regions to the pathomechanism of hepatic encephalopathy (HE), local cerebral metabolic rate for glucose (LCMRglue) was evaluated from [3H]-deoxyglucose uptake in frontal, visual and auditory cortex, striatum, cerebellum and medulla oblongata of rats with acute HE induced with a hepatotoxin--thioacetamide (TAA). HE caused a decrease of LCMRglue in all the regions studied. The strongest decrease (about 65%) was noted in hippocampus and cerebral cortex--the two regions rich in glutamatergic neurons. The results indicate a possible link between decreased energy metabolism and impaired excitatory, glutamatergic neurotransmission--the two factors whose contribution to HE has so far been implicated separately.
Hilgier
W
W
Department of Neuropathology, Polish Academy of Sciences, Warsaw.
Benveniste
H
H
Diemer
N H
NH
Albrecht
J
J
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D001921:Brain / Q000000981:diagnostic imaging / Q000187:drug effects / Q000378:metabolism*; D003847:Deoxyglucose / Q000378:metabolism; D005260:Female; D006501:Hepatic Encephalopathy / Q000139:chemically induced / Q000000981:diagnostic imaging / Q000378:metabolism*; D011877:Radionuclide Imaging; D051381:Rats; D011919:Rats, Inbred Strains; D012588:Scintillation Counting; D013853:Thioacetamide / Q000494:pharmacology*
D001786:Blood Glucose; D013853:Thioacetamide; D003847:Deoxyglucose