Influence of peripheral inflammation on the postnatal maturation of primary sensory neuron phenotype in rats.

The influence of early peripheral inflammation upon the postnatal development of rat primary sensory neuron subtypes was investigated. Lumbar dorsal root ganglia (DRG) were immunostained for calcitonin gene-related peptide (CGRP), neurofilament (NF200), and isolectin B4 (IB4) binding. Proportions of each subpopulation were measured at postnatal day (P) 0, P3, P7, and P21 in normal pups and in those that had received a unilateral hindpaw carrageenan injection at P1. The effects were compared with those following a similar injury in adults. Both the IB4 (positive [+ve]) and NF200+ve cell populations 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 stayed the same. After neonatal inflammation, the rise in IB4+ve binding occurred earlier but was the same as that in controls by P21. The CGRP+ve population 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 cells, but was normal by 3 weeks. Carrageenan in adults caused an increase in CGRP/IB4 cells only. The effects of peripheral inflammation differ in neonatal and adult DRG. Neonatal inflammation causes CGRP upregulation in both small and large cells and accelerates the postnatal increase in IB4 binding. These effects might influence subsequent central development.