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Title of Journal: J Neural Transm

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Abbravation: Journal of Neural Transmission

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Springer Vienna

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DOI

10.1016/0022-2011(69)90168-2

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ISSN

1435-1463

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Regionspecific causal mechanism in the effects of

Authors: Nobuyuki Maruoka Tetsuhito Murata Naoto Omata Hironori Mitsuya Yasushi Kiyono Hidehiko Okazawa Yuji Wada
Publish Date: 2012/11/04
Volume: 120, Issue: 3, Pages: 375-382
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Abstract

Ammonia which is considered to be the main agent responsible for hepatic encephalopathy inhibits oxidative glucose metabolism in the brain However the effects of ammonia on cerebral glucose metabolism in different brain regions remains unclear To clarify this issue we added ammonia directly to fresh rat brain slices and measured its effects on glucose metabolism Dynamic positron autoradiography with 18F2fluoro2deoxydglucose and 24iodophenyl34nitrophenyl524disulfophenyl2Htetrazolium WST1 colorimetric assay revealed that ammonia significantly increased the cerebral glucose metabolic rate and depressed mitochondrial function as compared to the unloaded control in each of the brain regions examined cerebral cortex striatum and cerebellum reflecting increased glycolysis that compensates for the decrease in aerobic metabolism Pretreatment with +5methyl1011dihydro5Hdibenzoadcyclohepten510imine hydrogen maleate MK801 a Nmethyldaspartate NMDA receptor antagonist significantly attenuated these changes induced by ammonia in cerebellum but not in cerebral cortex or striatum The addition of ammonia induced an increase in cyclic guanosine monophosphate cGMP levels in cerebellum but not in cerebral cortex or striatum reflecting the activation of the NMDA receptornitric oxidecGMP pathway These results suggested that NMDA receptor activation is responsible for the impairment of glucose metabolism induced by ammonia specifically in cerebellum

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