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. Author manuscript; available in PMC: 2013 Mar 1.
Published in final edited form as: Reg Anesth Pain Med. 2012 Mar;37(2):210–214. doi: 10.1097/AAP.0b013e31823b145f

Figure 1.

Figure 1

Immunoreactive µ-opioid receptor (MOR) in the ipsilateral dorsal horn of the lumbar spinal cord (A) and skin (B) at 4 weeks after topical hind paw infection with herpes simplex virus encoding the gene for the µOR in antisense (SGAMOR) or sense (SGMOR) direction relative to the cytomegalovirus promoter, or the viral control encoding [beta]-galactosidase (SGZ). A). MOR immunoreactivity is decreased in the ipsilateral L3 dorsal horn after SGAMOR infection (left panel) when compared with infection with the control SGZ virus (middle panel) while inoculation of the SGMOR viral vector results in increased MOR immunoreactivity in ipsilateral L3 dorsal horn (right panel). B) Quantitative changes in expression of MOR and overlapping immunoreactivity (-ir) with GFP in dorsal hind paw skin at 4 weeks after topical hind paw infection with herpes simplex virus. Compared with control SGZ infection, infection with SGAMOR decreases the number of MOR-ir afferent terminals in the epidermis of the medial dorsal hind paw skin. In contrast, infection with SGMOR increased the number of MOR-ir afferent terminals. Data are presented as average ± SD. *, *** P < 0.05, 0.001 compared with SGZ. (Adapted from Zhang et al 2008)55