Stress modulates GR activation after ischemic lesion. (A), GR nuclear density; (B), GR nuclear translocation. Lesion increased activated GR density in the lesion hemisphere compared to the non-lesion hemisphere in stress (A1 and A3) and control (A2 and A4) groups. Stress increased GR activation in the lesion hemisphere (A1) when compared to the non-lesion hemisphere (A3) (*p < 0.05). GR is constitutively expressed in the cytoplasm (arrow in B2), and inactive as a GR-HSP complex. GC enters the cell and binds to a GR dissociating the GR-HSP complex (Schema B3). Consequently, GR is activated when a GR-GC dimer is formed and translocated into the nucleus (arrow in B1; schema B3). Scale bars: 10 μm.