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Gamma-Aminobutyric Acid (GABA) and Sepsis-Related Encephalopathy

Published online by Cambridge University Press:  18 September 2015

T.R. Winder ,
G.Y. Minuk ,
E.J. Sargeant  and
T.P. Seland
T.R. Winder*
Affiliation:
Departments of Clinical Neurosciences and Medicine, University of Calgary
G.Y. Minuk
Affiliation:
Departments of Clinical Neurosciences and Medicine, University of Calgary
E.J. Sargeant
Affiliation:
Departments of Clinical Neurosciences and Medicine, University of Calgary
T.P. Seland
Affiliation:
Departments of Clinical Neurosciences and Medicine, University of Calgary
*
Reed Neurologic Institute, UCLA School of Medicine, Los Angeles, California, U.S.A. 90024
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Abstract:

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In order to determine whether disturbances in GABA homeostasis might play a role in the pathogenesis of sepsis-related encephalopathy, serum and brain tissue GABA concentrations from six areas of the brain (cortex, diencephalon, striatum, hippocampus, midbrain, and pons-medulla) were determined in a rat model of bacterial sepsis (cecal ligation and perforation). The results were compared to those obtained from sham operated control animals. All septic animals demonstrated clinical signs of encephalopathy and had elevated serum GABA levels (0.92 ± 0.3 uM versus 0.48 ± 0.15 in controls, p < 0.01). GABA content in the specific subcompartments of the brain, however, were similar in the two groups. These results indicate that although serum GABA levels are elevated during sepsis, GABA is unlikely to play an important role in the pathogenesis of sepsis-related encephalopathy.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 15 , Issue 1 , February 1988 , pp. 23 - 25
Copyright
Copyright © Canadian Neurological Sciences Federation 1988

References

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