Changes in corticosteroid hormone receptors in the ischemic gerbil hippocampal CA1 region following repeated restraint stress.

Restraint stress produces physiological changes including suppression of long-term potentiation in the brain. We observed the effects of repeated stress on ischemic damage associated with corticosteroid hormone receptors in gerbils. Animals were placed into restrainers for 5 h (between 09:30 h and 14:30 h) for 21 consecutive days prior to induction of transient cerebral ischemia. The animals were divided into 4 groups; (1) sham-operated-control-group (sham-group), (2) ischemia-operated-control-group (ischemia-group), (3) sham-operated-stress-group (stressed-sham-group), and (4) ischemia-operated-stress-group (stressed-ischemia-group). We found that serum corticosterone level in the ischemia-group was highest (374% of the sham-group) 12 h after ischemia/reperfusion and its level in the stressed-ischemia-group was significantly lower than the ischemia-group. Locomotor activity in the ischemia-group was significantly increased (295% of the sham-group) at 1 day post-ischemia; however, the locomotor activity in the stressed-ischemia-group was less increased compared to the ischemia-group. Cresyl violet positive (CV(+)) cells were significantly decreased in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) of the 4 days post-ischemia-group, while 79.4% of CV(+) cells were detected in the CA1 of the stressed-ischemia-group. Also, a few NeuN (neuron-specific soluble nuclear antigen)(+) cells were detected in the SP of the 4 days post-ischemia-group; however, in the 4 days stressed-post-ischemia-group, 77.2% of NeuN(+) neurons were found in the SP. Glial fibrillary acidic protein(+) astrocytes in the CA1 in the stressed-ischemia-groups were similar to those in the ischemia-groups; however, ionized calcium-binding adapter molecule 1(+) microglia in the stressed-ischemia-groups were less activated compared to the ischemia-groups. Mineralocorticoid receptor (MCR) and glucocorticoid receptor (GR) immunoreactivity in the SP of the stressed-ischemia-group were higher than the ischemia-group; at 4 days post-ischemia, MCR and GR immunoreactivity were expressed in non-pyramidal cells. In brief, our results indicate that repeated restraint stress significantly increase levels of corticosteroid hormone receptors and attenuates neuronal damage in the ischemic hippocampal CA1 region.