Time course of motor behavior changes in Mongolian gerbils submitted to different durations of cerebral ischemia

Janać, Branka; Radenović, Lidija; Selaković, Vesna; Prolić, Zlatko

doi:10.1016/j.bbr.2006.09.008

Cited by 52 publications

(34 citation statements)

References 25 publications

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“…We found that exposure to the repeated restraint stress significantly reduced the ischemia-induced spontaneous motor hyperactivity compared to the control ischemia-group. These results are supported by studies reported that decreases in corticosterone levels and spontaneous motor hyperactivity in the stressed-ischemia group is related to neuroprotection against ischemia damage [35,47].…”

Section: Discussionsupporting

confidence: 85%

“…On the other hand, Torres et al [45] reported that release of glucocorticoids following repeated exposure to a long stressful situation (40 days of exposure to restraint stress) decreased compared to that observed after the first exposure to this type of stress in rats. In addition, spontaneous motor activity, in our present study, has been used as a method to evaluate neuroprotection against ischemic damage in animals [35]. We found that exposure to the repeated restraint stress significantly reduced the ischemia-induced spontaneous motor hyperactivity compared to the control ischemia-group.…”

Section: Discussionmentioning

confidence: 88%

“…To examine the effects of chronic restraint stress against ischemia-induced hyperactivity, spontaneous motor activity in sham-, ischemia-, stressed-sham-and stressed-ischemiagroups was measured at designated times (1, 2, 3 and 4 days after the surgery) according to previous study [35]. For spontaneous motor activity, gerbils (n = 5 at each time point) were individually placed in a Plexiglas cage (25 cm 9 20 cm 9 12 cm), located inside a soundproof chamber.…”

Section: Spontaneous Motor Activitymentioning

confidence: 99%

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Changes in Corticosteroid Hormone Receptors in the Ischemic Gerbil Hippocampal CA1 Region Following Repeated Restraint Stress

et al. 2011

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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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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 88%

Section: Spontaneous Motor Activitymentioning

confidence: 99%

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Changes in Corticosteroid Hormone Receptors in the Ischemic Gerbil Hippocampal CA1 Region Following Repeated Restraint Stress

et al. 2011

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“…At the behavioral level, motor functions were evaluated by neurological disability status scale, locomotor activity and inclined beam-walking test. Cerebral ischemia is documented to impair motor ability and provoke pronounced motor hyperactivity, which is most prominent on the first postischemic day after ischemic damage (Araki et al, 2001;Janać et al 2006;Kuroiwa et al 1991;Rauš et al, 2012). Our findings are in accordance with the already published data.…”

Section: Discussionsupporting

confidence: 83%

5-HMF attenuates striatum oxidative damage via Nrf2/ARE signaling pathway following transient global cerebral ischemia

Hong-fang

Wang

et al. 2017

Cell Stress and Chaperones

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Recent studies have shown 5-hydroxymethyl-2-furfural (5-HMF) has favorable biological effects, and its neuroprotection in a variety of neurological diseases has been noted. Our previous study showed that treatment of 5-HMF led to protection against permanent global cerebral ischemia. However, the underlying mechanisms in cerebral ischemic injury are not fully understood. This study was conducted to investigate the neuroprotective effect of 5-HMF and elucidate the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway mechanism in the striatum after transient global cerebral ischemia. C57BL/6 mice were subjected to bilateral common carotid artery occlusion for 20 min and sacrificed 24 h after reperfusion. 5-HMF (12 mg/kg) or an equal volume of vehicle was intraperitoneally injected 30 min before ischemia and 5 min after the onset of reperfusion. At 24 h after reperfusion, neurological function was evaluated by neurological disability status scale, locomotor activity test and inclined beam walking test. Histological injury of the striatum was observed by cresyl violet staining and terminal deoxynucleotidyl transferase (TdT)-mediated dNTP nick end labeling (TUNEL) staining. Oxidative stress was evaluated by the carbonyl groups introduced into proteins, and malondialdehyde (MDA) levels. An enzyme-linked immunosorbent assay (ELISA)-based measurement was used to detect Nrf2 DNA binding activity. Nrf2 and its downstream ARE pathway protein expression such as heme oxygenase-1, NAD (P)H:quinone oxidoreductase 1, glutamate-cysteine ligase catalytic subunit and glutamate-cysteine ligase modulatory subunit were detected by western blot. Our results showed that 5-HMF treatment significantly ameliorated neurological deficits, reduced brain water content, attenuated striatum neuronal damage, decreased the carbonyl groups and MDA levels, and activated Nrf2/ARE signaling pathway. Taken together, these results demonstrated that 5-HMF exerted significant antioxidant and neuroprotective effects following transient cerebral ischemia, possibly through the activation of the Nrf2/ARE signaling pathway.

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“…To elucidate the effect of ND or HFD on ischemia-induced hyperactivity, spontaneous motor activity was measured at 1 day after ischemia-reperfusion according to previous studies [23]. For spontaneous motor activity, gerbils (n = 12 in each sham-groups, n = 36 in each ischemiagroups), were individually placed in a Plexiglas cage (25 cm 9 20 cm 9 12 cm), located inside a soundproof chamber.…”

Section: Spontaneous Motor Activitymentioning

confidence: 99%

Effects of High-Fat Diet on Neuronal Damage, Gliosis, Inflammatory Process and Oxidative Stress in the Hippocampus Induced by Transient Cerebral Ischemia

et al. 2014

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In this study, we investigated the effects of a normal diet (ND) and high-fat diet (HFD) on delayed neuronal death in the gerbil hippocampal CA1 region after transient cerebral ischemia. In the HFD-fed gerbils, ischemia-induced hyperactivity was significantly increased and neuronal damage was represented more severely compared to the ND-fed gerbils. Ischemia-induced glial activation was accelerated in the HFD-fed gerbils. Cytokines including interleukin-2 and -4 were more sensitive in the hippocampal CA1 region of the HFD-fed gerbils after ischemia-reperfusion. Additionally, we found that decreased 4-HNE and SODs immunoreactivity and protein levels in the hippocampal CA1 region of the HFD-fed gerbils after ischemia-reperfusion. These results indicate that HFD may lead to the exacerbated effects on ischemia-induced neuronal death in the hippocampal CA1 region after ischemia-reperfusion. These effects of HFD may be associated with more accelerated activations of glial cells and imbalance of pro- and anti-inflammatory cytokines and/or antioxidants after transient cerebral ischemia.

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Time course of motor behavior changes in Mongolian gerbils submitted to different durations of cerebral ischemia

Cited by 52 publications

References 25 publications

Changes in Corticosteroid Hormone Receptors in the Ischemic Gerbil Hippocampal CA1 Region Following Repeated Restraint Stress

Changes in Corticosteroid Hormone Receptors in the Ischemic Gerbil Hippocampal CA1 Region Following Repeated Restraint Stress

5-HMF attenuates striatum oxidative damage via Nrf2/ARE signaling pathway following transient global cerebral ischemia

Effects of High-Fat Diet on Neuronal Damage, Gliosis, Inflammatory Process and Oxidative Stress in the Hippocampus Induced by Transient Cerebral Ischemia

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