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Fig. 1. Egr3 expression is developmentally regulated and coupled to NGF
signaling in SCG neurons. (A) At E13, Egr3 expression was low in
SCG neurons and, by E15, Egr3 expression was markedly upregulated when
sympathetic neurons begin to express TrkA and to respond to NGF. Tyrosine
hydroxylase (TH) expression confirmed the representation of sympathetic
neurons in all of the RNA samples (results from five to eight pooled ganglia
for each developmental time point and qPCR performed in triplicate,
*P<0.001; n.s., no significant difference, Student's
t-test relative to E13 time point). (B) Egr3 expression was
not detectable at E13 by in situ hybridization, whereas at (C) birth
(P0) it was expressed by most, if not all SCG neurons. cs, carotid sinus; ca,
carotid artery; scg, superior cervical ganglion; scale bars: 100 µm.
(D) Treatment with NGF function-neutralizing antibody resulted in a 60%
reduction in Egr3 expression relative treatment with PBS, indicating that Egr3
expression was coupled to NGF signaling in SCG neurons in vivo (results from
n=5 PBS and NGF treated P0 mice and qPCR performed in triplicate;
**P<0.01, Mann-Whitney U test). (E) Egr3
expression was induced 
sixfold by NGF treatment, but not after treatment
with the neurotrophins NT4 or BDNF. NGF-dependent Egr3 induction was abrogated
using the MEK inhibitor U0126 (results from three experimental replicates and
qPCR performed in triplicate; *P<0.001, Student's
t-test relative to control).
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