Spinal cord of male wistar rats exposed to repeated psychological stress
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus Rattus norvegicus Homo sapiens
PROVIDER: GSE67832 | GEO | 2015/07/01
SECONDARY ACCESSION(S): PRJNA281010
REPOSITORIES: GEO
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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2015-07-01 | E-GEOD-67832 | biostudies-arrayexpress
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Project description:To test the effect of chronic water avoidance stress on spinal microRNA expression profile in male wistar rats.
2015-07-01 | GSE67831 | GEO
Project description:To test the effect of chronic water avoidance stress on spinal gene expression profile in male wistar rats. Lumbar spinal cord samples were freshly isolated from rats exposed to daily water avoidance stress for 10 consecutive days. Samples were collected 24 hours after the last stressors.
2015-07-01 | E-GEOD-67830 | biostudies-arrayexpress
Project description:To test the effect of chronic water avoidance stress on spinal microRNA expression profile in male wistar rats. Lumbar spinal cord samples were freshly isolated from rats exposed to daily water avoidance stress for 10 consecutive days. Samples were collected 24 hours after the last stressors.
2015-07-01 | E-GEOD-67831 | biostudies-arrayexpress
Project description:Toxicity evaluations of micro- or nano-sized plastics in rodent species commonly employed for toxicity analyses based on which risk assessment for humans could be performed are still largely lacking. Given this knowledge gap, the present work was aimed at determining the potential impact of chronic exposure to polystyrene nanoplastics (PS NPs) on the thyroid endocrine status and biochemical stress in a rat model. Young adult male rats were orally administered with PS NPs (1, 3, 6 and 10 mg kg-1 day-1) for five weeks. Thyroid hormones (THs) l-thyroxine (T4), l-triiodothyronine (T3), l-free triiodothyronine (FT3), and l-free thyroxine (FT4) as well as thyroid stimulating hormone (TSH) serum levels of normal rats and those exposed to PS NPs were compared. Serum levels of high-density lipoprotein (HDL), low-density lipoprotein (LDL), cholesterol, and creatinine, as well as glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) enzymes were also measured. Exposure to PS NPs suppressed the serum levels of T3 and circulating levels of THs, whereas TSH increased significantly. Though exposure to PS NPs did not affect the molar ratios of T3/T4, it induced a slight, but significant, increase in FT3/FT4. In addition, exposure to plastic nanoparticles showed signs of nephrotoxicity induction and kidney injury in exposed organisms as can be inferred from the significantly higher serum levels of creatinine in exposed groups. Our results provide clear evidence of an association between exposure to plastic NPs and thyroid endocrine disruption as well as metabolic deficit, and generate new leads for future research efforts.
| S-EPMC8142327 | biostudies-literature
Project description:Ketamine has gained significant attention as a fast-acting antidepressant. However, ketamine is also associated with undesirable side effects. In our preclinical study, we explored the behavioral effects of ketamine enantiomers at subanesthetic doses. During repeated intermittent treatment, we examined locomotor stimulation and sensitization, ataxia, and expression of natural behaviors (grooming and rearing). Male Wistar rats were subcutaneously treated repeatedly with either 5 mg/kg of R-ketamine or S-ketamine, 15 mg/kg of R-ketamine, S-ketamine or racemic ketamine, 30 mg/kg of racemic ketamine or saline every third day for three weeks (seven treatments overall). After the first treatment, only 15 mg/kg of S-ketamine induced locomotor stimulation, and both 15 mg/kg of S-ketamine and 30 mg/kg of racemic ketamine induced ataxia. Upon repeated administration, doses of 15 mg/kg of R-ketamine, S-ketamine, and racemic ketamine, as well as 30 mg/kg of racemic ketamine, stimulated locomotion. 15 mg/kg of R-ketamine, S-ketamine, and racemic ketamine additionally resulted in locomotor sensitization. The last administration of 15 mg/kg of S-ketamine, 15 mg/kg of racemic ketamine, and 30 mg/kg of racemic ketamine resulted in ataxia. In the case of 15 mg/kg of S-ketamine, ataxic effects were significantly weaker in comparison to the effects from the first administration, indicating tolerance. Natural behaviors were attenuated after 5 and 15 mg/kg of S-ketamine and 15 and 30 mg/kg of racemic ketamine. Neither of the R-ketamine doses produced such an effect. We conclude that S-ketamine has a stronger behavioral effect than R-ketamine.
| S-EPMC10906899 | biostudies-literature
Project description:There is strong evidence indicating that the social environment triggers changes to the psychological stress response and glucocorticoid receptor function. Considerable literature links the subsequent changes in stress resiliency to physical health. Here, converging evidence for the modulatory role of chronic psychological stress in the recovery process following spinal cord injury (SCI) is presented. Despite the considerable advances in SCI research, we are still unable to identify the causes of variability in patients' recovery following injury. We propose that individuals' past and present life experiences (in the form of stress exposure) may significantly modulate patients' outcome post-SCI. We propose a theoretical model to explain the negative impact of chronic psychological stress on physical and psychological recovery. The stress experienced in life prior to SCI and also as a result of the traumatic injury, could compromise glucocorticoid receptor sensitivity and function, and contribute to high levels of inflammation and apoptosis post-SCI, decreasing the tissue remaining at the injury site and undermining recovery of function. Both stress-induced glucocorticoid resistance and stress-induced epigenetic changes to the glucocorticoid receptor can modulate the nuclear factor-kappa B regulated inflammatory pathways and the Bcl-2 regulated apoptosis pathways. This model not only contributes to the theoretical understanding of the recovery process following injury, but also provides concrete testable hypotheses for future studies.
| S-EPMC3988397 | biostudies-other
Project description:BackgroundSpinal cord injury (SCI) induces a multitude of deleterious processes, including neuroinflammation and oxidative stress (OS) which contributed to neuronal damage and demyelination. Recent studies have suggested that increased formation of reactive oxygen species (ROS) and the consequent OS are critical events associated with SCI. However, there is still little information regarding the impact of these events on SCI. Astrocytes are key regulators of oxidative homeostasis in the CNS and astrocytic antioxidant responses promote the clearance of oxidants produced by neurons. Therefore, dysregulation of astrocyte physiology might largely contribute to oxidative damage. Nuclear factor erythroid 2-related factor 2 (Nrf2) is the main transcriptional regulator of cellular anti-oxidative stress responses.MethodsIn the current study, we hypothesized that astrocytic activation of Nrf2 protects the spinal cord post injury via suppression of neuroinflammation. Thus, using mice line with a GFAP-specific kelch-like ECH-associated protein 1 (Keap1)-deletion, we induced a hyperactivation of Nrf2 in astrocytes and further its effects on SCI outcomes. SCI-induction was performed in mice using the Infinite Horizon Spinal Cord Impactor with a force of 60 kdyn. To assess the quantitative pattern of Nrf2/ARE-activation, we included transgenic ARE-Luc mice. Data were analyzed with GraphPad Prism 8 (GraphPad Software Inc., San Diego, CA, USA). Brown-Forsythe test was performed to test for equal variances and normal distribution was tested with Shapiro-Wilk.ResultsIn ARE-Luc mice, a significant induction of luciferase-activity was observed as early as 1 day post-injury, indicating a functional role of Nrf2-activity at the epicenter of SCI. Furthermore, SCI induced loss of neurons and oligodendrocytes, demyelination and inflammation in wild type mice. The loss of myelin and oligodendrocytes was clearly reduced in Keap1 KO mice. In addition, Keap-1 KO mice showed a significantly better locomotor function and lower neuroinflammation responses compared to wild type mice.ConclusionsIn summary, our in vivo bioluminescence data showed Nrf2-ARE activation during primary phase of SCI. Furthermore, we found that cell specific hyperactivation of Nrf2 was sufficient to protect the spinal cord against injury which indicate a promising therapeutic approach for SCI-treatment.
| S-EPMC9169394 | biostudies-literature
Project description:The blood-spinal cord barrier (BSCB) plays significance roles in recovery following spinal cord injury (SCI), and diabetes mellitus (DM) impairs endothelial cell function and integrity of BSCS. Endoplasmic reticulum (ER) stress occurs in the early stages of SCI and affects prognosis and cell survival. However, the relationship between ER stress and the integrity of BSCB in diabetic rats after SCI remains unclear. Here we observed that diabetic rats showed increased extravasation of Evans Blue (EB) dye, and loss of endothelial cells and pericytes 1?day after SCI compared to non-diabetic rats. Diabetes was also shown to induce activation of ER stress. Similar effects were observed in human brain microvascular endothelial cells. 4-phenylbutyric acid (4-PBA), an ER stress inhibitor lowered the adverse effect of diabetes on SCI, reduced EB dye extravasation, and limited the loss of endothelial cells and pericytes. Moreover, 4-PBA treatment partially reversed the degradation of tight junction and adherens junction both in vivo and in vitro. In conclusion, diabetes exacerbates the disruption of BSCB after SCI via inducing ER stress, and inhibition of ER stress by 4-PBA may play a beneficial role on the integrity of BSCB in diabetic SCI rats, leading to improved prognosis.
| S-EPMC5550423 | biostudies-literature