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Nerve growth factor‐stimulated mitogen‐activated protein kinase activity is not necessary for neurite outgrowth of chick dorsal root ganglion sensory and sympathetic neurons
Author(s) -
Klinz Franz Josef,
Wolff Peter,
Heumann Rolf
Publication year - 1996
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/(sici)1097-4547(19961215)46:6<720::aid-jnr8>3.0.co;2-h
Subject(s) - dorsal root ganglion , neurite , nerve growth factor , protein kinase a , sensory system , microbiology and biotechnology , mitogen activated protein kinase , sensory neuron , sympathetic ganglion , dorsum , ganglion , neuroscience , biology , chemistry , kinase , anatomy , in vitro , receptor , biochemistry
Nerve growth factor (NGF)‐stimulated neurite outgrowth in the rat PC12 tumor cell line recently has been shown to depend on the activation of the mitogen‐activated protein (MAP) kinase kinase 1 (MEK1) (Pang et al.: J Biol Chem 270:13585–13588, 1995). In this study we have analyzed whether or not function of the MAP kinase pathway is necessary for NGF‐stimulated neurite outgrowth in two subtypes of primary neurons derived from the embryonic chick peripheral nervous system (PNS). Treatment of p21ras‐dependent dorsal root ganglion (DRG) sensory neurons (E9) with the MEK1 inhibitor PD98059 at concentrations up to 100 μM did not prevent NGF‐stimulated neurite outgrowth. At this concentration NGF‐stimulated tyrosine phosphorylation of MAP kinase p42 as well as MAP kinase activity both were decreased by approximately 80%. Essentially the same results were obtained with p21ras‐independent sympathetic neurons (E12). We conclude that, in contrast to the PC12 tumor cell line, NGF‐stimulated MAP kinase activity is not necessary for neurite outgrowth of DRG sensory and sympathetic neurons derived from the chick PNS. © 1996 Wiley‐Liss, Inc.