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The Journal of Neuroscience, February 15, 1998, 18(4):1230-1239

Calmodulin Is Involved in Membrane Depolarization-Mediated Survival of Motoneurons by Phosphatidylinositol-3 Kinase- and MAPK-Independent Pathways

Rosa M. Soler, Joaquim Egea, Gerard M. Mintenig, Cesar Sanz-Rodriguez, Montse Iglesias and Joan X. Comella

Grup de Neurobiologia Molecular, Departament de Ciències Mèdiques Bàsiques, Facultat de Medicina, Universitat de Lleida, 25198 Lleida, Catalonia, Spain

In the present work, we find that the elevation of extracellular K⁺ concentration promotes the survival of chick spinal cord motoneurons in vitro deprived of any neurotrophic support. This treatment induces chronic depolarization of the neuronal plasma membrane, which activates L-type voltage-dependent Ca²⁺ channels, resulting in Ca²⁺ influx and elevation of the cytosolic free Ca²⁺ concentration. Pharmacological reduction of intracellular free Ca²⁺ or withdrawal of extracellular Ca²⁺ reversed the effects of depolarization on survival. The intracellular Ca²⁺ response to membrane depolarization developed as an initial peak followed by a sustained increase in intracellular Ca²⁺ concentration. The depolarizing treatment caused tyrosine phosphorylation of mitogen-activated protein kinase (MAPK) without involving tyrosine kinase receptor activation. The calmodulin antagonist W13 inhibited the survival-promoting effect induced by membrane depolarization but not the tyrosine phosphorylation of MAPK. Moreover, depolarization did not induce phosphatidylinositol-3 kinase (PI-3K) phosphorylation in our cells, and the PI-3K inhibitor wortmannin did not suppress the survival-promoting effect of K⁺ treatment. These results suggest that calmodulin is involved in calcium-mediated survival of motoneurons through the activation of PI-3K- and MAPK-independent pathways.

Key words: motoneuron; calmodulin; signal transduction; trophic factor; depolarization; apoptosis

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Copyright © 1998 Society for Neuroscience  0270-6474/98/1841230-10$05.00/0

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