THE ACTIVATION OF CALCIUM CALMODULIN-DEPENDENT PROTEIN-KINASE-II AFTER GLUTAMATE OR POTASSIUM STIMULATION IN HIPPOCAMPAL SLICES/

Two forms of long-term potentiation (LTP), N-methyl-D-aspartate recept or (NMDAR) dependent and non-NMDAR dependent, have been reported in hi ppocampal CA1 and CA3, respectively. The present study examined the ac tivati on of CaM-kinase II (calcium/calmodulin - dependent protein kin ase II) in CA1 and CA3 areas after glutamate or potassium stimulation, Rat hippocampal slices were preincubated with one of the drugs (EGTA, DL-APV, CNQX, AP3, nitrendipine, KN-62, staurosporin, and H-89) befor e they were stimulated with either glutamate/glycine (100 mu M/1 mu M) or KCl (60 mM). Hippocampal CA1 area and CA3 area were then dissected and CaM-kinase II activities were assayed in vitro. Glutamate and KCI stimulations enhanced the percentage of Ca2+-independent CaM-kinase I I activity in CA1 area. This enhancement was suppressed by EGTA, DL-AP V, CNQX, or KN-62, suggesting that the neuronal stimulation effect in CA1 area was mediating through NMDA receptors. Conversely, there was n o significant enhancement of CaM-kinase II activity in the CA3 area af ter glutamate or KCI stimulation. Nevertheless, the percentage of calc ium-independent CaM-kinase II activity in the CA3 area was suppressed by EGTA, nitrendipine, KN-62, staurosporin, or H-89, indicating that t he activity of CaM-kinase II in the CA3 area was independent of NMDA r eceptor activation. (C) 1997 Elsevier Science Inc.