title: Role of glutamate receptors and an on-going protein synthesis in the regulation of phosphorylation of Ca2+/calmodulin-dependent protein kinase II in the CA3 hippocampal region in mice administered with kainic acid intracerebroventricularly.
abstract: In an immunohistochemical study, kainic acid (KA, 0.1 microg) administered intracerebroventricularly (i.c.v.) dramatically increased the expression of Ca2+/calmodulin-dependent protein kinase II (CaMK II) and the phosphorylation of CaMK II (p-CaMK II) in the CA3 hippocampal region of mice. Pre-treatment with cycloheximide (a protein synthesis inhibitor; 200 mg/kg) intraperitoneally prevented the expression of CaMK II and phosphorylation of CaMK II induced by KA. In addition, pre-treatment with MK-801 ((5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine; an NMDA receptor blocker, 1 microg, i.c.v.) or CNQX (6-cyano-7-nitroquinoxaline-2,3-dione; a non-NMDA receptor blocker, 0.5 microg, i.c.v.) attenuated the p-CaMK II, but not CaMK II, expression induced by KA. Our results suggest that KA administered supraspinally induces CaMK II and the phosphorylation of CaMK II expression in the CA3 hippocampal region, for which an on-going protein synthesis is needed. Furthermore, both NMDA and non-NMDA receptors appear to be involved in supraspinally administered KA-induced phosphorylation of CaMK II.
authors.affiliation: Department of Pharmacology, Institute of Natural Medicine, College of Medicine, Hallym University, 1 Okchun-Dong, Chunchon, Kangwon-Do, 200-702, South Korea.
authors.forename: Han-Kyu
authors.initials: HK
authors.lastname: Lee
authors.forename: Seong-Soo
authors.initials: SS
authors.lastname: Choi
authors.forename: Eun-Jung
authors.initials: EJ
authors.lastname: Han
authors.forename: Ki-Jung
authors.initials: KJ
authors.lastname: Han
authors.forename: Hong-Won
authors.initials: HW
authors.lastname: Suh
mesh_terms: D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000096:biosynthesis* / Q000187:drug effects*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D006624:Hippocampus / Q000187:drug effects* / Q000201:enzymology / Q000503:physiopathology; D007276:Injections, Intraventricular; D007608:Kainic Acid / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009474:Neurons / Q000187:drug effects* / Q000201:enzymology; D009498:Neurotoxins / Q000494:pharmacology*; D010766:Phosphorylation / Q000187:drug effects; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D017470:Receptors, Glutamate / Q000187:drug effects* / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
chemical_list: D018691:Excitatory Amino Acid Antagonists; D009498:Neurotoxins; D011500:Protein Synthesis Inhibitors; D017470:Receptors, Glutamate; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D007608:Kainic Acid