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Increase in Neurite Formation and Acetylene line Release by Transfection of Growth‐Associated Protein‐43 cDNA into NG108–15 Cells

Abstract: We previously reported that growth‐associated protein‐43 (GAP‐43) could be involved in the maintenance of elongated neurites and that a decline in protein kinase C activity may be involved in accumulation of GAP‐43. In the present study, to clarify the functional significance of GAP‐43 for neurite maintenance and acetylcholine (ACh) release, we prepared NG‐G11 cells by transfection of GAP‐43 cDNA into NG108‐15 cells. NG‐G11 cells expressed GAP‐43 mRNA at levels approximately twice that in nontransfected or vector‐transfected cells under control conditions and after treatment with dibutyryl cyclic AMP (diBu‐cAMP) or 12‐O‐tetradecanoylphorbol 13‐acetate (TPA) plus diBu‐cAMP. Neurite outgrowth after addition of diBu‐cAMP was greater in NG‐G11 than in control cells. In NG‐G11 cells, neurites elongated by treatment with diBu‐cAMP for 72 h were maintained after removal of the drug. Treatment with TPA plus diBu‐cAMP for 24 h induced neurite outgrowth in NG‐G11 cells, although control cells required 72 h. Depolarization by 50 mM KCI induced ACh release in both NG‐G11 and control cells treated with diBu‐cAMP or TPA/diBu‐cAMP. Although removal of the drugs following diBu‐cAMP treatment reversed ACh release to nontreated levels in control cells, a high‐K+‐induced level of ACh release remained in NG‐G11 cells after removal of diBu‐cAMP. ACh release induced by TPA plus diBu‐cAMP for 24 h was further enhanced after removal of the drugs in NG‐G11 cells, but it was not seen in control cells. These results suggest that levels of GAP‐43 mRNA are correlated with neurite maintenance and the level of ACh release. Thus, GAP‐43 may be involved in neuronal differentiation in NG108‐15 cells.