||Acquisition and Loss of a Neuronal Ca(2+)/Calmodulin-Dependent Protein Kinase during Neuronal Differentiation.
Jensen, K. F. ;
Ohmstede, C. A. ;
Fisher, R. S. ;
Olin, J. K. ;
Sahyoun, N. ;
||Health Effects Research Lab., Research Triangle Park, NC. Neurotoxicology Div. ;Wellcome Research Labs., Research Triangle Park, NC. ;California Univ., Los Angeles. School of Medicine. ;NSI Technology Services Corp., Research Triangle Park, NC.;Public Health Service, Rockville, MD.
||EPA/600/J-91/134; PHS-HD05958 ;PHS-NS24596;
Protein kinases ;
Purkinje cells ;
Western blotting ;
Electron microscopy ;
||Some EPA libraries have a fiche copy filed under the call number shown.
Calcium ions play a critical role in neural development. Insights into the ontogeny of Ca(2+)-signaling pathways were gained by investigating the developmental expression of granule cell-enriched Ca(2+)/calmodulin-dependent protein kinase (CaM kinase-Gr) in the cerebellum and hippocampus of the rat. Neurons of these brain regions displayed characteristic schedules by which they acquired and displayed characteristic schedules by which they acquired and lost CaM kinase-Gr during differentiation. In the cerebellum, granule cells did not begin to express CaM kinase-Gr until after birth when they migrated into the granule cell layer, and the expression persisted in the adult. Purkinie cells expressed CaM kinase-Gr prenatally and lost this expression by postnatal day 14. In contrast, the granule and pyramidal cells of the hippocampus expressed the enzyme prenatally and in the adult.