Iba1 expression following ICH and blockade or stimulation of the EP1 receptor. Antagonist (SC-51089, 10 µg/kg), agonist (17-pt-PGE2, 0.3 mg/kg), or vehicle (saline) was administered subcutaneously at the onset of injury, 6 h post-ICH, and at 12-h intervals thereafter. Seventy-two hours after ICH, brains were harvested and sections processed for Iba1 immunohistochemistry to evaluate cortical and striatal microgliosis. a, b Representative high magnification photomicrographs showing the ipsilateral and contralateral a cortex and b striatum for Iba1 immunohistochemistry of coronal brain sections from control (left panels), SC-51089- (middle panels), and 17-pt-PGE2- (right panels) treated mice. Square selections in the insets denote magnified regions. Scale bars on the magnified images and insets are 100 µm and 2 mm, respectively. c, d Quantification of Iba1 immunoreactivity demonstrated that SC-51089-treated mice had significantly more c cortical microgliosis, whereas no significant differences were seen in (d) striatal microgliosis. This increased cortical Iba1 immunoreactivity was accompanied by more cellular morphological changes. No significant differences in c cortical or d striatal microgliosis were seen for the 17-pt-PGE2-treated mice. Data is normalized to the corresponding contralateral equivalent signal with appropriate control for the area of quantification in striatal analyses (see “Methods”). *p < 0.05 when compared to the control group, n = 8–10 per group.