title: Comparison of effects induced by toxic applications of kainate and glutamate by glucose deprivation on area CA1 of rat hippocampal slices.
abstract: Baseline and stimulus-induced changes in [Ca2+]o and [K+]o as well as field potentials (fp's) were studied during application of the excitatory amino acids kainate or glutamate, or during glucose deprivation in area CA1 and CA3 of rat hippocampal slices. Bath application of kainate in concentrations of 1, 2, 5, 8 and 10 mM induced a sudden rapid fall of [Ca2+]o in area CA1, associated with a negative shift of the slow fp. Kainate induced disappearance of stratum radiatum (SR) as well as alveus stimulation-evoked postsynaptic fp's, with partial recovery after application of up to 2 mM kainate, but no recovery after 5 mM kainate. Only afferent volleys and repetitive SR stimulation-induced decreases of [Ca2+]o recovered after 5 mM kainate. Similar observations were made with glutamate. Only when glutamate was applied with 20 mM, irreversible disappearance of postsynaptic fp's was noted. Glucose deprivation for 60-90 min led to an initial slow decline of [Ca2+]o in area CA1 and CA3, associated with increases in [K+]o, but no significant changes in the fp baseline. Before reaching the lowest level in [Ca2+]o, stimulation of afferent and efferent fibres in area CA1 and CA3 evoked epileptiform discharges. After reaching the lowest level in [Ca2+]o, all postsynaptic potential components were irreversibly abolished, sparing afferent volleys and SR stimulation-induced decreases in [Ca2+]o. The application of the glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 30 microM) and L-2-amino-5-phosphonovalerate (2AVP, 30 microM) during glucose deprivation did not prevent irreversible loss of alveus and SR stimulation-induced postsynaptic signals. These findings suggest that glutamate release during glucose deprivation is not the main factor of acute cell damage.
authors.affiliation: Department Neurophysiology, Charité, Medical School, Humboldt University Berlin, Germany. alici@charite.hu-berlin.de
authors.forename: K
authors.initials: K
authors.lastname: Alici
authors.forename: T
authors.initials: T
authors.lastname: Gloveli
authors.forename: G
authors.initials: G
authors.lastname: Weber-Luxenburger
authors.forename: V
authors.initials: V
authors.lastname: Motine
authors.forename: U
authors.initials: U
authors.lastname: Heinemann
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000378:metabolism; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000172:deficiency*; D018698:Glutamic Acid / Q000506:poisoning*; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism*; D066298:In Vitro Techniques; D007608:Kainic Acid / Q000506:poisoning*; D008297:Male; D009994:Osmolar Concentration; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
chemical_list: D018691:Excitatory Amino Acid Antagonists; D018698:Glutamic Acid; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D015763:2-Amino-5-phosphonovalerate; D005947:Glucose; D011188:Potassium; D007608:Kainic Acid; D002118:Calcium