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

Abstract

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.

• Authors: Ki-Yeon Yoo, Choong Hyun Lee, Jung Hoon Choi, Youdong Sohn, Jun Hwi Cho, In Koo Hwang, Young-Myeong Kim, Moo-Ho Won
• Journal: Neurochemical research (Neurochem Res) Vol. 36 Issue 5 Pg. 701-12 (May 2011) ISSN: 1573-6903 [Electronic] United States
• PMID: 21207139 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Receptors, Steroid
• Corticosterone

Topics

• Animals
• Blotting, Western
• Brain Ischemia (metabolism)
• Corticosterone (blood)
• Gerbillinae
• Hippocampus (metabolism, pathology)
• Immobilization
• Immunohistochemistry
• Male
• Motor Activity
• Receptors, Steroid (metabolism)
• Stress, Physiological