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- Title
Regulation of Voltage-Dependent Sodium Channel Expression in Adrenal Chromaffin Cells.
- Authors
KOBAYASHI, HIDEYUKI; SHIRAISHI, SEIJI; YANAGITA, TOSHIHIKO; YOKOO, HIROKI; YAMAMOTO, RYUICHI; MINAMI, SHIN-ICHI; SAITOH, TOMOKAZU; WADA, AKIHIKO
- Abstract
A bstract: The density and electrical activity of cell surface voltage-dependent Na+ channels are key determinants regulating the neuronal plasticity including development, differentiation, and regeneration. Abnormalities of Na+ channels are associated with various neurological diseases. In this paper, we review the regulatory mechanisms of cell surface Na+ channel expression mediated by Ca2+ signaling pathways in cultured bovine adrenal chromaffin cells. Sustained, but not transient, elevation of intracellular Ca2+ concentration reduced the number of cell surface Na+ channels. The reduction of Na+ channels was suppressed by an inhibitor of calpain, a Ca2+-dependent protease, and by an inhibitor of protein kinase C (PKC). The activation of conventional PKC-α and novel PKC-ε reduced cell surface Na+ channels by the acceleration of internalization of the channels and by the increased degradation of Na+ channel α-subunit mRNA, respectively. On the contrary, the activation of PKC-ε increased Na+ channel β1-subunit mRNA level. The inhibition of calcineurin, a Ca2+/calmodulin-dependent protein phosphatase 2B, by immunosuppressants upregulated cell surface Na+ channels by both stimulating externalization and inhibiting internalization of the channels without changing Na+ channel α- and β1-subunit mRNA levels. Thus, the signal transduction pathways mediated by intracellular Ca2+ modulate cell surface Na+ channel expression via multiple Ca2+-dependent events, and the changes in the intracellular vesicular trafficking are the important mechanisms in the regulation of Na+ channel expression.
- Publication
Annals of the New York Academy of Sciences, 2002, Vol 971, Issue 1, p127
- ISSN
0077-8923
- Publication type
Article
- DOI
10.1111/j.1749-6632.2002.tb04446.x