Fig. 3.
Confocal microscopy of double immunofluorescence of mineralocorticoid receptor (MR; red fluorescence) with microglia marker OX-42 or astrocyte marker glial fibrillary acidic protein (GFAP) (green fluorescence) in spinal cord sections of Freund’s complete adjuvant (FCA)–treated rats versus controls (Ctrl). (A, B, E, and F) Most of MR immunoreactivity (red) is devoid of colocalization with OX-42 or GFAP (green) in the spinal dorsal horn of FCA-treated rats versus controls (bar = 40 µm). (C, D, G, and H) Quantitative analysis shows that the number of reactive OX-42–immunoreactive (ir) microglia as well as GFAP-ir astrocytes was significantly increased in FCA-treated rats compared to controls without a significant increase in the colocalization of OX-42–ir and GFAP-ir cells with MR (P < 0.05, two-tailed independent Student’s t test). Data are expressed as mean ± SD. Act. = activated; IOD = integrated optical density.

Confocal microscopy of double immunofluorescence of mineralocorticoid receptor (MR; red fluorescence) with microglia marker OX-42 or astrocyte marker glial fibrillary acidic protein (GFAP) (green fluorescence) in spinal cord sections of Freund’s complete adjuvant (FCA)–treated rats versus controls (Ctrl). (A, B, E, and F) Most of MR immunoreactivity (red) is devoid of colocalization with OX-42 or GFAP (green) in the spinal dorsal horn of FCA-treated rats versus controls (bar = 40 µm). (C, D, G, and H) Quantitative analysis shows that the number of reactive OX-42–immunoreactive (ir) microglia as well as GFAP-ir astrocytes was significantly increased in FCA-treated rats compared to controls without a significant increase in the colocalization of OX-42–ir and GFAP-ir cells with MR (P < 0.05, two-tailed independent Student’s t test). Data are expressed as mean ± SD. Act. = activated; IOD = integrated optical density.

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