B. Beland et M. Fitzgerald, Influence of peripheral inflammation on the postnatal maturation of primary sensory neuron phenotype in rats, J PAIN, 2(1), 2001, pp. 36-45
The influence of early peripheral inflammation upon the postnatal developme
nt of rat primary sensory neuron subtypes was investigated. Lumbar dorsal r
oot ganglia (DRG) were immunostained for calcitonin gene-related peptide (C
GRP), neurofilament (NF200), and isolectin B4 (IB4) binding. Proportions of
each subpopulation were measured at postnatal day (P) 0, P3, P7, and P21 i
n normal pups and in those that had received a unilateral hindpaw carrageen
an injection at P1. The effects were compared with those following a simila
r injury in adults. Both the IB4 (positive [+ve]) and NF200+ve cell populat
ions increased postnatally (IB4+ve: 23 +/- 1.6% to 32.6 +/- 1.3%; NF200+ve:
33.8 +/- 1.2% to 43.3 +/- 1.9%), whereas the population of CGRP+ve cells s
tayed the same. After neonatal inflammation, the rise in IB4+ve binding occ
urred earlier but was the same as that in controls by P21. The CGRP+ve popu
lation increased at 2 and 6 days after carrageenan in neonates, because of
an increase in both small CGRP/IB4 and larger CGRP/NF200 double-labeled cel
ls, but was normal by 3 weeks. Carrageenan in adults caused an increase in
CGRP/IB4 cells only. The effects of peripheral inflammation differ in neona
tal and adult DRG. Neonatal inflammation causes CGRP upregulation in both s
mall and large cells and accelerates the postnatal increase in IB4 binding.
These effects might influence subsequent central development.