Changes in Corticosteroid Hormone Receptors in the Ischemic Gerbil Hippocampal CA1 Region Following Repeated Restraint Stress |
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| Authors: | Ki-Yeon Yoo Choong Hyun Lee Jung Hoon Choi Youdong Sohn Jun Hwi Cho In Koo Hwang Young-Myeong Kim Moo-Ho Won |
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| Institution: | (1) Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea;(2) Laboratory of Veterinary Pharmacology, College of Veterinary Medicine, Seoul National University, Seoul, 151-742, South Korea;(3) Department of Anatomy, College of Veterinary Medicine, Kangwon National University, Chuncheon, 200-701, South Korea;(4) Department of Emergency Medicine, Hallym University Sacred Heart Hospital, College of Medicine, Hallym University, Anyang, 431-070, South Korea;(5) Department of Emergency Medicine, Kangwon National University Hospital, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea;(6) Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science, Seoul National University, Seoul, 151-742, South Korea;(7) Vascular System Research Center and Department of Molecular and Cellular Biochemistry, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea;(8) Institute of Medical Sciences, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea; |
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| 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. |
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