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Nerve Growth Factor is Required for Induction of c‐Fos Immunoreactivity by Serum, Depolarization, Cyclic AMP or Trauma in Cultured Rat Sympathetic Neurons
Author(s) -
Buckmaster A.,
Nobes C. D.,
Edwards S. N.,
Tolkovsky A. M.
Publication year - 1991
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1991.tb00855.x
Subject(s) - nerve growth factor , depolarization , stimulation , c fos , microinjection , endocrinology , medicine , immediate early gene , neurite , period (music) , chemistry , sympathetic ganglion , biology , neuroscience , gene expression , in vitro , gene , receptor , biochemistry , physics , acoustics
Nerve growth factor (NGF) induces transient Fos‐immunoreactivity (Fos‐IR) independently of any other factor, both in newly isolated rat sympathetic neurons and in established cultures after NGF deprivation. The same proportion of neurons that express Fos‐IR in response to NGF also survive. In addition to direct stimulation of Fos‐IR expression, the presence or recent exposure to NGF is required to obtain Fos‐IR expression by other stimuli. In newly isolated neurons no Fos‐IR is detected in response to stimulation by serum alone and a response to depolarization or cyclic AMP is obtained only if neurons are stimulated within a short period after ganglion excision. In established cultures none of these stimuli, nor the trauma of cutting neurites or spiking cell bodies with a microinjection needle induce Fos‐IR unless NGF is present or had been removed for <8–16 h. The lack of response is not due to a general decrease in the rate of protein or RNA synthesis. These findings show that in regenerating sympathetic neurons NGF induces c‐Fos and suggest that NGF may activate a master trigger that is required for c‐Fos expression to be induced by other stimuli.