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. 2014 Mar 11;9(3):e91297. doi: 10.1371/journal.pone.0091297

Figure 3. Up-regulation of GABAB2 receptor expression in superficial laminae of the spinal cord after chronic oxycodone treatment.

Figure 3

A–C: Immunofluorescent staining showing GABAB2 receptor labelling in the dorsal horn in (A) vincristine-saline, (B) vincristine-morphine, and (C) vincristine-oxycodone treated animals. D: Analysis of the fluorescence intensity profiles of GABAB2 receptor immunoreactivity from superficial to deeper layers in control/vincristine treated animals chronically treated with saline, morphine or oxycodone. The selected zone was a vertical area in laminae I through IV (white selection in A). The insert shows the mean fluorescent intensity ± SEM in the three groups of vincristine-treated rats as mean ± SEM. For ease of reading, it was not possible to show the SEM of all groups. E: Mean fluorescent intensity of GABAB2 receptor immonoreactivity at the level of the first 50 μm of the spinal cord dorsal horn. Vincristine treatment did not alter the intensity of GABAB2 receptor staining as compared to saline-treated animals. However, oxycodone (but not morphine) significantly increased the intensity of GABAB2 receptor staining in the superficial lamina. (n = 4 vincristine-morphine treated rats; n = 4 saline-morphine treated rats), (n = 4 vincristine-oxycodone treated rats; n = 4 saline-oxycodone treated rats), and (n = 4 vincristine-saline treated rats; n = 4 saline-saline treated rats) *p<0.05 and **p<0.01 vincristine-oxycodone vs. vincristine-morphine. Data are expressed as mean ± SEM.