Glucocorticoid receptor expression in the cortex of the neonatal rat brain with and without focal cerebral ischemia.

BACKGROUND/AIMS Glucocorticoid receptors (GR) mediate cellular processes which may be neuroprotective and/or neurotoxic to the neonatal rat brain. Our aim was to describe GR ontogeny in the developing rat brain cortex and changes in GR expression after permanent neonatal focal cerebral ischemia (FCI). METHODS GR Western blots and immunohistochemical stains were performed on neonatal rat cortices on P1, P3, P7, P10, P15, and P30 and on P7 at 1 h, 3 h, 6 h, 12 h, 24 h, and 72 h after FCI or sham-operation (S-O), 8 per group. Nissl staining was performed on FCI or S-O P7 cortical samples. RESULTS Cortical GR expression was increased by 65.2% at P7, 110.1% at P15, and 87.0% at P30, compared to P1. On P7, GR expression decreased in the ischemic cortex after 6 h and in the non-ischemic cortex after 24 h of FCI (p < 0.05). Cortical GR expression was not altered in S-O P7 rats. Immunohistochemistry supported Western blot findings. Nissl staining revealed no gross decrease in neuronal number in non-ischemic cortices after 24 h of FCI, compared to baseline. CONCLUSIONS Neonatal rat cortical GR expression increases during P1 to P30, peaking at P15. At P7, cortical GR expression appears downregulated in the ischemic cortex after 6 h and in the non-ischemic cortex after 24 h of FCI. Thus, cortical GR may play important roles in normal brain development and neonatal brain injury responses.