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Co‐activation of insulin‐like growth factor‐I receptors and protein kinase C results in parasympathetic neuronal survival
Author(s) -
Crouch M. F.,
Hendry I. A.
Publication year - 1991
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490280112
Subject(s) - endocrinology , medicine , receptor , insulin , protein kinase c , growth factor , biology , activator (genetics) , insulin like growth factor , insulin receptor , kinase , microbiology and biotechnology , insulin resistance
We have studied the interaction between several growth factors to promote parasympathetic neuronal survival. Neither insulin nor insulin‐like growth factor‐I (IGF‐I) had any effect on the survival of embryonic day 8 chick ciliary neurons in culture. Similarly, the protein kinase C activator phorbol dibutyrate (PdBu) had only a minor survival‐promoting activity. In combination with PdBu, however, IGF‐I or insulin, at concentrations sufficient to act through the IGF‐I receptor, were highly synergistic. In a similar fashion, acidic fibroblast growth factor (aFGF)‐induced neuronal survival was greatly enhanced by PdBu, as well as by insulin or IGF‐I. When added alone, aFGF‐induced cell survival required the presence of 1% serum. However, addition of aFGF, IGF‐I, or insulin with PdBu under serum‐free conditions replaced the serum requirement. That is, these agonist combinations could apparently induce the second messenger requirement for ciliary neuronal survival. Therefore, IGF‐I must now be included in the list of candidate molecules responsible for directing parasympathetic nerve formation. The synergy between agonists observed in these experiments highlights the possibility that combinations of growth factors, rather than sole molecules, may dictate parasympathetic nervous system development in vivo.