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Decreased glucose utilization in discrete brain regions of rat in thioacetamide‐induced hepatic encephalopathy as measured with [ 3 H]‐deoxyglucose
Author(s) -
Hilgier W.,
Benveniste H.,
Diemer N. H.,
Albrecht J.
Publication year - 1991
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1991.tb03961.x
Subject(s) - deoxyglucose , glutamatergic , thioacetamide , striatum , cerebellum , hippocampus , cerebral cortex , hepatic encephalopathy , endocrinology , neuroscience , medicine , chemistry , encephalopathy , cortex (anatomy) , excitatory postsynaptic potential , medulla oblongata , glutamate receptor , biology , central nervous system , cirrhosis , receptor , dopamine , inhibitory postsynaptic potential
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 (LCMR gluc ) was evaluated from [ 3 H]‐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 LCMR gluc 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.