Figure 3
GCSF increased mu opioid receptor (MOR)-positive axons in the injured sciatic nerve.
Representative images of double immunofluorescence for MOR (red) and calcitonin gene related peptide (CGRP), a marker of peptidergic small to medium size neurons (green; (A)); NF200, heavy subunit of neuro-filament (green; (B)); and S100, β-subunit of Schwann cell (green; (C)) in the injured sciatic nerve of the sham controls, vehicle-treated CCI rats and GCSF-treated CCI rats on the 3rd day after nerve injury. (D) Quantification of MOR-positive axons in the injured sciatic nerve of sham controls, vehicle-treated CCI and GCSF-treated CCI rats. A significantly higher number of MOR-positive axons were observed in GCSF-treated CCI rats than in vehicle-treated CCI rats (P < 0.05). The MOR-positive axons in the injured sciatic nerve were also slightly higher in vehicle-treated CCI rats than in the sham control rats (P < 0.05). Most MORs were co-stained with CGRP-positive axons and S100-positive Schwann cells. There were only a few MOR-positive stained cells co-localized with N200-positive axons. Scale bars = 20 μm. The data are shown as the mean ± SEM. #P < 0.05, ##P < 0.01: GCSF-treated or vehicle-treated groups compared to sham-operated controls. *P < 0.05, **P < 0.01: GCSF-treated CCI groups compared to vehicle-treated CCI groups. Kruskal–Wallis, post hoc Mann–Whitney rank-sum test (n = 4, in each group). Arrowheads indicate CGRP-positive/MOR-positive axons. Some S100-positive/MOR-positive cells were also observed.
