Global cerebral ischemia (GCI) causes extensive neuronal injury and significant behavioural impairments. Although these sequelae can be mitigated by selective activation of estrogen receptors (ERs), their influence on inflammatory processes mediated by microglial activation are not fully understood. This study characterized the impact of selective ER activation on post-ischemic anxiety-like behaviours and microglial activation. 46 adult female Wistar rats were ovariectomized and, starting the following day, received daily subcutaneous injections of propylpyrazole triol (ERα agonist), diarylpropionitrile (ERβ agonist), G-1 (G-protein coupled ER agonist; GPER), 17β-Estradiol (E2; activating all receptors), or vehicle solution (VEH) for 21 days (all 100 μg/kg/day). Rats then underwent GCI or a sham surgery (n=6, received vehicle injections). The Elevated Plus Maze (EPM) and Hole Board Test (HBT) assessed anxiety-like behaviours. Thionine staining measured neuronal survival, while immunofluorescence assessed microglial activation (Iba1, CD68) in the basolateral amygdala (BLA), CA1 of the hippocampus, and paraventricular nucleus of the hypothalamus (PVN). All ischemic groups except for DPN had lower neuronal density and increased CA1 Iba1 microglial activation than shams. Compared to shams, both PPT and VEH rats displayed increased anxiety-like behaviours in the EPM and impaired emotion regulation (decreased grooming) in the HBT, associated with higher Iba1 expression in the PVN of PPT rats. E2 rats also displayed impaired emotion regulation in the HBT compared to shams and G-1, which coincided with G-1 rats having lower CD68 in the BLA. Overall, these results highlight several ER specific impacts on anxiety-like behaviours and microglial activation despite minimal neuroprotection.