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Journal of Neuroscience, Vol 15, 2081-2096, Copyright © 1995 by Society for Neuroscience
Differential influence of nerve growth factor on neuropeptide expression in vivo: a novel role in peptide suppression in adult sensory neurons
VM Verge, PM Richardson, Z Wiesenfeld-Hallin and T Hokfelt
Department of Anatomy, University of Saskatchewan, Saskatoon, Canada.
In this study the actions of NGF in regulating peptide expression were
examined in vivo in adult rat primary sensory neurons. The hypothesis that
NGF might tonically inhibit expression of some peptides was tested
specifically. In situ hybridization and immunohistochemistry were used to
detect presence or absence of alpha-CGRP, beta-CGRP, SP, SOM, VIP, CCK,
NPY, and GAL as well as their mRNAs. In neurons in normal lumbar DRG
alpha-CGRP, beta-CGRP, SP, and SOM are abundantly and heterogeneously
expressed whereas few neurons have detectable VIP, CCK, NPY, or GAL. Two
weeks following sciatic nerve transection, concentrations of alpha-CGRP,
beta-CGRP, SP, and SOM plus their mRNAs have decreased to background in all
but a few neurons. In contrast, VIP, CCK, NPY, and GAL are now synthesized
in many neurons. Delayed intrathecal infusion of NGF (125 ng/microliter/hr)
for 7 d, starting 2 weeks after injury counteracted the decrease in
expression of alpha- CGRP, beta-CGRP and SP expression, but not SOM. This
lack of influence of NGF on SOM is consistent with the absence of
high-affinity NGF receptors and trk mRNA in SOM-positive neurons. Delayed
infusion of NGF also reduced the number of neurons expressing VIP, CCK,
NPY, and GAL after injury by approximately one-half in each subpopulation.
Therefore, we suggest that NGF suppresses expression of these four peptides
but only if the neurons also have NGF receptors. The results show that NGF
can regulate peptide expression differentially and may also be part of the
signal that allows reversion to normal of responses to injury as axons
regenerate.
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