title: Extracellular acidic sulfur-containing amino acids and gamma-glutamyl peptides in global ischemia: postischemic recovery of neuronal activity is paralleled by a tetrodotoxin-sensitive increase in cysteine sulfinate in the CA1 of the rat hippocampus.
abstract: An excessive activation of the excitatory amino acid system has been proposed as one possible mediator of the ischemia-induced delayed death of CA1 pyramidal cells in the hippocampus. Using dialytrodes in the CA1 of the rat, we have investigated multiple-unit activity and extracellular changes in acidic sulfur-containing amino acids and gamma-glutamyl peptides during ischemia (20-min, four-vessel occlusion) and during 8 h of reflow. Multiple-unit activity was abolished during ischemia and for the following 1 h, but then recovered, gradually reaching preischemic levels after 8 h of reflow. Extracellular cysteate, cysteine sulfinate, and gamma-glutamyltaurine increased (1.5- to threefold) during ischemia, and extracellular glutathione and gamma-glutamylaspartate plus gamma-glutamylglutamine increased during early reflow (two- to threefold). The recovery of neuronal activity at 4-8 h was paralleled by an increase in extracellular cysteine sulfinate (2.5-fold at 8 h of reflow). Perfusion with 10 microM tetrodotoxin at 8 h of reflow abolished the multiple-unit activity and reduced extracellular cysteine sulfinate. Considering the glutamate-like properties of cysteine sulfinate, the observed postischemic increase may be involved in the development of the delayed neuronal death.
authors.affiliation: Institute of Neurobiology, University of Göteborg, Sweden.
authors.forename: P
authors.initials: P
authors.lastname: Andiné
authors.forename: O
authors.initials: O
authors.lastname: Orwar
authors.forename: I
authors.initials: I
authors.lastname: Jacobson
authors.forename: M
authors.initials: M
authors.lastname: Sandberg
authors.forename: H
authors.initials: H
authors.lastname: Hagberg
mesh_terms: D000143:Acids / Q000378:metabolism; D000596:Amino Acids / Q000378:metabolism*; D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism*; D003545:Cysteine / Q000031:analogs & derivatives / Q000378:metabolism; D004151:Dipeptides / Q000378:metabolism; D004563:Electrochemistry; D005110:Extracellular Space / Q000378:metabolism; D005973:Glutamine / Q000031:analogs & derivatives / Q000378:metabolism; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000502:physiology; D018377:Neurotransmitter Agents; D051381:Rats; D011919:Rats, Inbred Strains; D013455:Sulfur / Q000378:metabolism*; D013654:Taurine / Q000031:analogs & derivatives / Q000378:metabolism; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D000143:Acids; D000596:Amino Acids; D004151:Dipeptides; D018377:Neurotransmitter Agents; D005973:Glutamine; C047442:gamma-glutamylglutamine; C021030:gamma-glutamylaspartic acid; D013654:Taurine; D013779:Tetrodotoxin; D013455:Sulfur; C020903:glutaurine; D003545:Cysteine; C013461:cysteine sulfinic acid