title: [Effect of excitatoxicity on Ca2+/CaM PK II activity in rat hippocampal slices].
abstract: The relation between Ca2+/CaM PK II activity and excitatoxicity was studied in an in vitro model of rat hippocampal slices. The slices were exposed to 50-200 mumol.L-1 glutamate or 25-100 mumol.L-1 NMDA and glucose-free Krebs buffer for 30 min after being recovered to normal conditions by 2 hours of incubation with standard Krebs buffer. The results showed that inhibition of Ca2+/CaM PK II activity in rat hippocampal slices was induced by exogenous EAA (glutamate or NMDA), and Ca2+/CaM PK II activity values decreased to 50.1% and 44.7% of control at 200 mumol.L-1 glutamate and 100 mumol.L-1 NMDA, respectively; MK801, but not DNQX, antagonized EAA-induced inhibition of Ca2+/CaM PK II activity. When the slices were pretreated with MK801 prior to exposure to 200 mumol.L-1 glutamate or 100 mumol.L-1 NMDA, the Ca2+/Cam PK II activity values were 91.5% and 96.7%, respectively. The changes of extracellular Ca2+ or Mg2+ concentration influenced Ca2+/CaM PK II activity of the slices exposed to exogenous glutamate; Ca2+/CaM PK II activity values in the presence of extracellular Ca2+ was lower than that in the absence of extracellular Ca2+, and it changed from 50.1% of control (presence of Ca2+) to 64% of control (absence of Ca2+) at 200 mumol.L-1 glutamate, but Ca2+/CaM PK II activity values in the presence of extracellular Mg2+ was higher than that in the absence of extracellular Mg2+, and it changed from 50.1% of control(presence of Mg2+) to 36.6% of control (absence of Mg2+) at 200 mumol.L-1 glutamate. The results suggest that NMDA receptor may be involved in excitotoxicity-induced inhibition of Ca2+/CaM PK II activity.
authors.affiliation: Research Center of Biochemistry and Molecular Biology, Xuzhou Medical College, Xuzhou 221002.
authors.forename: X
authors.initials: X
authors.lastname: Feng
authors.forename: Y
authors.initials: Y
authors.lastname: Zong
authors.forename: G
authors.initials: G
authors.lastname: Zhang
mesh_terms: D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism*; D016291:Dizocilpine Maleate / Q000494:pharmacology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000494:pharmacology; D006624:Hippocampus / Q000201:enzymology*; D066298:In Vitro Techniques; D008297:Male; D016202:N-Methylaspartate / Q000494:pharmacology; D018696:Neuroprotective Agents / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors
chemical_list: D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D018696:Neuroprotective Agents; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D016202:N-Methylaspartate; D016291:Dizocilpine Maleate; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases