Figure 3

The CCR2 chemokine receptor colocalized with IB ₄ and TRPV1, markers of nociceptive neurons, after injury. A) Many lumbar DRG neurons in vehicle-treated rat sensory neurons were positive for IB₄, a neuronal phenotype that distinguishes some C-fiber nociceptors (red cells), however there was no expression of the CCR2 protein. B) After perineural gp120/hCD4 treatment, CCR2 protein expression (green cells) was upregulated, and co-localized with IB₄. C) Both gp120/hCD4 and ddC treatment resulted in an upregulation of CCR2 expression (green cells) in many small and medium diameter neurons. Again, CCR2 co-localized in a number of IB₄ positive cells. D) The TRPV1 channel is present on many nociceptive neurons and is involved in the neuropathic pain mechanism. Under normal conditions, TRPV1 was expressed in neurons (red cells). E) After gp120/hCD4 treatment, CCR2 expression is upregulated (green cells) and colocalized with TRPV1. F) After the combination of gp120/hCD4 and ddC treatments, again CCR2 was upregulated to a similar degree as gp120/hCD4 treatment alone and exhibited some colocalizations with TRPV1. G) The percentage of CCR2-positive cells that co-localized with IB₄ and TRPV1. CCR2 receptor expression was upregulated after gp120/hCD4 alone and the combination of gp120/hCD4 and ddC treatments. Most cells were of small and medium diameter. Approximately half of the CCR2-positive cells also colocalized with IB₄ or TRPV1. Sham treatment did not result in an upregulation of CCR2 protein expression. IB4 and TRPV1 were expressed in all conditions, and did not differ significantly between groups. Yellow arrows: colocalizing neurons; white arrows: non-colocalizing neurons. Data represents mean ± SE. Scale Bar: 100 um.