Hyperammonemic alterations in the uptake and release of glutamate and aspartate by rat cerebellar preparations.
Release and uptake of neurotransmitter amino acids, glutamate and aspartate, were studied in the synaptosomes, astrocytes and in the perikarya of granule neurons isolated from the cerebella of normal and hyperammonemic rats. During acute hyperammonemia, depolarization-induced release of both the amino acids from the synaptosomes was elevated. The Vmax values of high-affinity uptake systems were elevated without alterations in the Km values for these two amino acids during acute hyperammonemic states. In the case of the low-affinity uptake system of these two amino acids, there was a decrease in the Km values without alterations in the Vmax values. These results are discussed in relation to the mechanism of ammonia toxicity.
School of Life Sciences, University of Hyderabad, India.
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Rao
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Murthy
D000641:Ammonia / Q000097:blood*; D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism*; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism; D002531:Cerebellum / Q000166:cytology / Q000378:metabolism*; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D007700:Kinetics; D008560:Membrane Fluidity / Q000187:drug effects; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism
D005971:Glutamates; D009419:Nerve Tissue Proteins; D001224:Aspartic Acid; D018698:Glutamic Acid; D011189:Potassium Chloride; D000641:Ammonia