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.

Acupuncture treatment for post-stroke depression: Intestinal microbiota and its role

“…Moreover, the HPA axis, as one of the key components of stress regulation, can timely perceive pressure and quickly initiate signals in the paraventricular nucleus (PVN) of the hypothalamus, and HPA axis abnormalities may be one of the biological indicators for depression in its early stages ( Spalletta et al, 2006 ; Du and Pang, 2015 ). Moreover, there is evidence that acute ischemic stroke can act as a stressor to activate the HPA axis ( Wexler, 1970 ; Yoo et al, 2011 ). There are several basic studies showing that acupuncture can down-regulate the expression of CRH mRNA in hypothalamus, reduce plasma levels of ACTH and CORT ( Le et al, 2016 ; Zheng et al, 2019 ), which plays an antidepressant role by inhibiting the over-excitation of HPA axis ( Han X. et al, 2021 ).…”