Neuroactive amino acids and glutamate (NMDA) receptors in frontal cortex of rats with experimental acute liver failure

✍ Scribed by A Michalak; C Rose; J Butterworth; R F Butterworth

• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 257 KB
• Volume: 24
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.510240425

✦ Synopsis

cephalopathy in acute liver failure. For example, studies in It has been proposed that alterations of excitatory and experimental animals with either ischemic or thioacetamideinhibitory amino acids play a role in the pathogenesis induced acute liver failure reveal decreased levels of excitof hepatic encephalopathy in acute liver failure. To evalatory amino acids (glutamate, aspartate) in brain 2,3 ; CSF uate this possibility, in vivo cerebral microdialysis was concentrations of these amino acids were concomitantly inused to sample extracellular concentrations of amino creased. No changes were found in brain or CSF concentraacids in the frontal cortex of unanesthetized rats at varitions of g-aminobutyric acid (GABA) in either ischemic or ous times during the progression of encephalopathy rethioacetamide-induced acute liver failure. 3 Similar negative sulting from acute liver failure. Liver failure was inresults were reported for GABA in autopsied brain tissue duced by portacaval anastomosis followed 24 hours later from patients with acute liver failure. 4

Abbreviations: CSF, cerebrospinal fluid; GABA, g-aminobutyric acid; NMDA; N-methylchased from Amersham (Arlington Heights, IL). D-aspartate; HPLC, high-performance liquid chromatography; SH, shunt; SM, sham; HAL, Surgical Techniques. Male Sprague-Dawley rats (weighing 175hepatic artery ligation.