Activation of Ca (2+) /calmodulin-dependent protein kinase Ii in cerebellar granule cells by N-methyl-d-aspartate receptor activation
Fukunaga, K.; Soderling, T.R.
Molecular and Cellular Neurosciences 1(2): 133-138
ISSN/ISBN: 1044-7431 PMID: 19912763 DOI: 10.1016/1044-7431(90)90017-x
Cultured cerebellar granule cells were studied to determine if the excitatory neurotransmitter glutamate acting through the N-methyl-d-aspartate (NMDA) receptor could stimulate autophosphorylation of Ca(2+)/calmodulin-dependent protein kinase II (CaM-kinase II) to generate its Ca(2+)-independent form. Glutamate did elevate Ca(2+)-independent CaM-kinase II through autophosphorylation when granule cells were incubated in Mg(2+)-free buffer, and this response was potentiated by 1 muM glycine. Extracellular Ca(2+) was required, and specific antagonists of the NMDA receptor blocked the response. These results support the hypothesis that postsynaptic Ca(2+) influx through the NMDA receptor-gated ion channel, as occurs during induction of long-term potentiation, may convert CaM-kinase II to a constitutively active, Ca(2+)-independent form.