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The Effect of the B Subunit of Cholera Toxin on the Action of Nerve Growth Factor on PC12 Cells
Author(s) -
Mutoh Tatsuro,
Tokuda Akira,
Guroff Gordon,
Fujiki Norio
Publication year - 1993
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1993.tb03319.x
Subject(s) - nerve growth factor , cholera toxin , microbiology and biotechnology , neurite , biology , ganglioside , cytochalasin b , intracellular , receptor , endocrinology , biochemistry , cell , in vitro
Exogenous gangliosides, especially ganglioside GM1 (GM1), seem to potentiate the action of nerve growth factor (NGF). We have examined the possible regulation of the NGF signaling pathway in PC12 cells by the B subunit of cholera toxin (CTB), which binds to endogenous GM1 specifically and with a high affinity. CTB treatment (1 μg/ml) enhanced NGF‐induced neurite outgrowth from PC12 cells, NGF‐induced activation of ribosomal protein S6 kinase, and NGF‐induced stimulation of trk phosphorylation. CTB plus NGF also caused a greater inhibition of [ 3 H]‐thymidine incorporation into DNA than did NGF alone. These enhancing effects of CTB were blocked by the presence of cytochalasin B in the culture medium but were not affected by the presence of colchicine or by the depletion of Ca 2+ in the medium. 125 I‐NGF binding experiments revealed that CTB treatment did not affect the specific binding of NGF to the cells. These results strongly suggest that the binding of cell surface GM1 by CTB modulates the pathway of intracellular signaling initiated by NGF and that the association of CTB with a cytoskeletal component is essential for these effects.