Amino acid release from cerebral cortex in experimental acute liver failure, studied by in vivo cerebral cortex microdialysis.

Abstract:

:Both increased gamma-aminobutyric acid (GABA)-ergic and decreased glutamatergic neurotransmission have been suggested relative to the pathophysiology of hepatic encephalopathy. This proposed disturbance in neurotransmitter balance, however, is based mainly on brain tissue analysis. Because the approach of whole tissue analysis is of limited value with regard to in vivo neurotransmission, we have studied the extracellular concentrations in the cerebral cortex of several neuroactive amino acids by application of the in vivo microdialysis technique. During acute hepatic encephalopathy induced in rats by complete liver ischemia, increased extracellular concentrations of the neuroactive amino acids glutamate, taurine, and glycine were observed, whereas extracellular concentrations of aspartate and GABA were unaltered and glutamine decreased. It is therefore suggested that hepatic encephalopathy is associated with glycine potentiated glutamate neurotoxicity rather than with a shortage of the neurotransmitter glutamate. In addition, increased extracellular concentration of taurine might contribute to the disturbed neurotransmitter balance. The observation of decreasing glutamine concentrations, after an initial increase, points to a possible astrocytic dysfunction involved in the pathophysiology of hepatic encephalopathy.

journal_name

J Neurochem

authors

Bosman DK,Deutz NE,Maas MA,van Eijk HM,Smit JJ,de Haan JG,Chamuleau RA

doi

10.1111/j.1471-4159.1992.tb09410.x

keywords:

subject

Has Abstract

pub_date

1992-08-01 00:00:00

pages

591-9

issue

2

eissn

0022-3042

issn

1471-4159

journal_volume

59

pub_type

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