title: Activation of Ca(2+)/calmodulin-dependent protein kinase II in cerebellar granule cells by N-methyl-d-aspartate receptor activation.
abstract: 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.
authors.affiliation: Department of Molecular Physiology and Biophysics Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA.
authors.forename: K
authors.initials: K
authors.lastname: Fukunaga
authors.forename: T R
authors.initials: TR
authors.lastname: Soderling