Effect Of Chronic Immobilization Stress Research Articles

Morphological changes of the exocrine part of the pancreas under immobilization stress on the background of hypothyrosis

Annotation. Stress is a condition that causes the body's cells to use large amounts of energy to acclimate to abnormal environmental conditions. Hypothyroidism affects almost all organs and systems of the body, in particular, the pancreas. The goal of our research is to study the effect of chronic immobilization stress against the background of hypothyroidism on the tissue structure of the exocrine part of the pancreas. The experimental rats were divided into three groups: I – intact animals (10), II – animals with immobilization stress (10), III – animals with hypothyroidism and immobilization stress (10). Hypothyroidism was modeled by daily per os injection using a probe of the pharmacopoeial mercazolil thyreostatics at a dose of 25 mg/kg during the 21 day. Acute immobilization stress was modeled by tying experimental rats in a supine position in 4 limbs without restriction of head mobility for 3 hours. Histological studies were carried out according to generally accepted methods. Histological preparations were studied using a SEO SСAN light microscope and photo-documented using a Vision CCD Camera with a system of image output from histological preparations. In the 1st control group, the pancreas had a general structure plan of a parenchyme in organ. In the II group, remodeling of the exocrine part of the pancreas, slight disturbances in the structure of the acini, blood vessels, and moderate edema of the connective tissue were observed, compared to the control group of animals. In the III group, more significant changes of the gland were revealed, compared to the II experimental group, manifested by swelling and growth of connective tissue, changes in the shape of the acini, violation and loss of polarity of exocrinocytes, blood-filling of vessels. Thus, under conditions of simulated chronic stress, slight changes in the parenchyma of the gland were detected, and during chronic immobilization stress against the background of hypothyroidism, alterative changes of the gland were detected, compared to the II experimental group.

Sex differences impact the pancreatic response to chronic immobilization stress in rats.

Chronic stress has been related to multiple diseases. Inflammation is proposed strongly to link stress to stress-related diseases in different organs, such as small intestine, colon, and brain. However, stress cellular effect on the pancreatic tissue, especially the exocrine one, had received relatively little attention. This work aimed to evaluate the cellular effect of chronic immobilization stress on the pancreatic tissue function and structure along with evaluating the sex role in this type of pancreatic injury. Thirty rats were equally divided into 5 groups: control male, control female, stressed male, stressed female, and stressed female with bilateral ovariectomy. Stressed rats were exposed to immobilization for 1 h/day, 6 days/week, for 3 weeks. Rats were then decapitated for further biochemical, histological, histo-morphometric, and immunohistochemical study. The results showed that, in male and female rats, chronic immobilization stress produced hypoinsulinemia and hyperglycemia, with increasing exocrine pancreatic injury markers by increasing oxidative and inflammatory status of the pancreatic tissue, and exhibited a degenerative effect on the pancreatic tissue. However, the stress-induced pancreatic effects were more obvious in male rats and female rats with bilateral ovariectomy than that in female rats. It could be concluded that male animals were more susceptible to stress-induced pancreatic damage than females. The ovarian hormones are responsible, at least partly, for pancreatic tissue protection since the stress-induced pancreatic injury in females was exacerbated by ovariectomy. In this study, inflammatory and oxidative stress differences in both sexes could provide a plausible explanation for sex differences.

Effects of chronic immobilization stress on biokinetics and dosimetry of 67Ga in a murine model.

The aim of this work is to determine the effect of chronic immobilization stress on kinetics and dosimetry of 67Ga in a mouse model. A control group (CG) and a stress group (SG), each with 15 mice, were included in the study, and the latter group was subjected to a chronic immobilization stress model 2h daily for 14 consecutive days. At day 13, 67Ga-citrate was administered intraperitoneally (11.24 ± 0.44MBq) to each mouse. Then, sets of three mice were obtained sequentially at 24, 36, 48, 60 and 72h, in which the radionuclide activity was measured with an activity counter. The 67Ga biokinetic data showed a fast blood clearance in the SG, with a mean residence time of 0.06h. The calculated mean radiation absorbed doses were: liver (2.45 × 10-03 Gy), heart (3.17 × 10-04 Gy) and kidney (1.88 × 10-04 Gy) in the SG. The results show that stress reduced weight gain by approximately 13% and also increased adrenal gland weight by 26%. On the other hand, chronic stress accelerates 67Ga clearance after 24h compared to normal conditions. It is concluded that murine organisms under chronic immobilization stress have higher gallium-67 clearance rates, decreasing the cumulated activity and absorbed dose in all organs.

Effect of chronic immobilization stress on the pancreatic structure and the possible protective role of testosterone administration in male albino rats

Effect of chronic immobilization stress on the pancreatic structure and the possible protective role of testosterone administration in male albino rats

The effect of chronic immobilization stress on leptin signaling in the ovariectomized (OVX) rat

Previous studies have shown that both 17β-estradiol (E2) treatment and chronic stress may attenuate post-OVX weight gain in the female rat. However, the interaction between E2 and stress is unclear. This study examined the effect of E2 treatment and chronic immobilization stress on body weight. Adult OVX Sprague-Dawley rats were randomly assigned to one of four treatment groups in a 2X2 factorial design examining hormone treatment [vehicle (VEH) or E2, sc] and stress (no stress vs stress 60 min/day for 22 days). After 22 days, E2 significantly inhibited weight gain and food intake in OVX rats. In contrast, chronic stress reduced body weight only in control OVX animals but did not affect food intake. E2 reduced circulating leptin levels in non-stressed animals, but not in animals subjected to chronic immobilization. Western blot analysis indicated that E2 treatment increased leptin receptor (Ob-Rb) expression in the medial basal hypothalamus (MBH); however, this treatment also increased suppressor of cytokine signaling 3 (SOCS3), which is an inhibitor of leptin signaling. Chronic immobilization stress blunted the E2-induced increase in Ob-Rb and SOCS3 levels. These results suggest that chronic stress counteracts E2 effects on leptin signaling in the MBH without altering body weight.

Chronic stress-induced changes in REM sleep on theta oscillations in the rat hippocampus and amygdala

The present study investigated the effect of Chronic Immobilization Stress (CIS) on theta oscillations in the hippocampus and amygdala during Rapid Eye Movement (REM) sleep. Adult male Wistar rats were subjected to 2h of CIS daily for 10days. Polysomnographic recordings with electroencephalogram (EEG) from hippocampus (CA3 and CA1 subregion) and lateral nucleus of amygdala (LA) were carried out after termination of CIS protocol on the 7th, 14th and 21st day. The results showed a bimodal distribution on the total REM sleep duration in CIS rats: group of rats exhibited increased REM sleep duration considered as a stress-enhanced REM (SER) and rats with reduced REM sleep as stress-reduced REM sleep (SRR) group. The bimodal distribution in REM sleep was continued to exhibit even after 21 days of termination of stress, showing increased REM sleep in SER and reversible REM sleep in SRR rats. In addition to changes in sleep, increased REM sleep in SER rats was associated with attenuated theta activity in the hippocampus and amygdala, while the SRR rats did not show attenuated theta activities during the stress recovery period. Thus, the study demonstrates the dependence of synchronized amygdalo-hippocampal theta activity with the CIS-induced enhanced REM sleep duration. This raises the possibility that CIS-induced manifestations of the anxiety may be associated with synchronized theta oscillations in the hippocampus and amygdala.

Restraint stress increases neuroinflammation independently of amyloid β levels in amyloid precursor protein/PS1 transgenic mice

Both hypercortisolemia and hippocampal damage are features found in patients diagnosed of Alzheimer's disease (AD) and epidemiological evidence supports a role for stress as a risk factor for AD. It is known that immobilization stress is followed by accumulation of oxidative/nitrosative mediators in brain after the release of proinflammatory cytokines, nuclear factor kappa B activation, nitric oxide synthase-2 and cyclooxygenase-2 expression. Long-term exposure to elevated corticosteroid levels is known to affect the hippocampus which plays a central role in the regulation of the hypothalamic-pituitary-adrenal axis. We therefore studied the effect of chronic immobilization stress on amyloid precursor protein/PS1 mice. Stress exposure increased AD-induced neuroinflammation characterized by astrogliosis, increased inflammatory gene transcription and lipid peroxidation. Importantly, immobilization stress did not increase the soluble or insoluble amyloid β levels suggesting that increased cortisol levels lower the threshold for a neuroinflammatory response, independently from amyloid β. Since inflammation may act as a factor that contributes disease progression, the stress-inflammation relation described here may be relevant to understand the initial mechanisms in underlying the risk enhancing action of stress on AD.

Changes of Glucocorticoid Receptor and Levels of CRF mRNA, POMC mRNA in Brain of Chronic Immobilization Stress Rats

The effect of chronic immobilization stress (CIS) on the biochemical parameters has been one of the hot topics in neuroscience. The aim of this study was to investigate the effects of CIS on the levels of glucocorticoid receptor (GR), corticotrophin-releasing factor (CRF) mRNA and proopiomelanocortin (POMC) mRNA in brains of rats. The rats were randomly divided into stressed and control groups. The stressed group was given CIS 3 h a day for 21 days continuously. GR of rats' hippocampus and prefrontal cortex (PFC) were detected by immunohistochemistry method. In addition, the CRF mRNA and POMC mRNA of rats' brain regions (hypothalamus, pituitary, hippocampus, and PFC) were detected by reverse transcription-polymerase chain reaction (RT-PCR). After exposure to CIS for 21 days, the GR immuno staining (the gray values) of the stressed group was less than that of the control group in hippocampal CA(1), dentate gyrus, and PFC (P < 0.01). Quantitative analysis indicated the presence of CRF mRNA in hypothalamus and pituitary, while POMC mRNA in PFC, hippocampus and pituitary of the stressed group was less than that of the control group (P < 0.01). The decreased levels of GR, CRF mRNA, and POMC mRNA in different brain regions may contribute to explanation of the CIS induced mechanism.

Chronic stress decreases the expression of sympathetic markers in the pineal gland and increases plasma melatonin concentration in rats

Chronic stress affects brain areas involved in learning and emotional responses. Although most studies have concentrated on the effect of stress on limbic-related brain structures, in this study we investigated whether chronic stress might induce impairments in diencephalic structures associated with limbic components of the stress response. Specifically, we analyzed the effect of chronic immobilization stress on the expression of sympathetic markers in the rat epithalamic pineal gland by immunohistochemistry and western blot, whereas the plasma melatonin concentration was determined by radioimmunoassay. We found that chronic stress decreased the expression of three sympathetic markers in the pineal gland, tyrosine hydroxylase, the p75 neurotrophin receptor and alpha-tubulin, while the same treatment did not affect the expression of the non-specific sympathetic markers Erk1 and Erk2, and glyceraldehyde-3-phosphate dehydrogenase. Furthermore, these results were correlated with a significant increase in plasma melatonin concentration in stressed rats when compared with control animals. Our findings indicate that stress may impair pineal sympathetic inputs, leading to an abnormal melatonin release that may contribute to environmental maladaptation. In addition, we propose that the pineal gland is a target of glucocorticoid damage during stress.

Chronic stress induces upregulation of brain-derived neurotrophic factor (BDNF) mRNA and integrin α5 expression in the rat pineal gland

Chronic stress affects brain areas involved in learning and emotional responses. These alterations have been related with the development of cognitive deficits in major depression. Moreover, stress induces deleterious actions on the epithalamic pineal organ, a gland involved in a wide range of physiological functions. The aim of this study was to investigate whether the stress effects on the pineal gland are related with changes in the expression of neurotrophic factors and cell adhesion molecules. Using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot, we analyzed the effect of chronic immobilization stress on the BDNF mRNA and integrin α5 expression in the rat pineal gland. We found that BDNF is produced in situ in the pineal gland. Chronic immobilization stress induced upregulation of BDNF mRNA and integrin α5 expression in the rat pineal gland but did not produce changes in β-actin mRNA or in GAPDH expression. Stressed animals also evidenced an increase in anxiety-like behavior and acute gastric lesions. These results suggest that BDNF and integrin α5 may have a counteracting effect to the deleterious actions of immobilization stress on functionally stimulated pinealocytes. Furthermore, this study proposes that the pineal gland may be a target of glucocorticoid damage during stress.

Chronic stress impairs acoustic conditioning more than visual conditioning in rats: Morphological and behavioural evidence

Chronic stress affects brain areas involved in learning and emotional responses. These alterations have been related with the development of cognitive deficits in major depression. The aim of this study was to determine the effect of chronic immobilization stress on the auditory and visual mesencephalic regions in the rat brain. We analyzed in Golgi preparations whether stress impairs the neuronal morphology of the inferior (auditory processing) and superior colliculi (visual processing). Afterward, we examined the effect of stress on acoustic and visual conditioning using an avoidance conditioning test. We found that stress induced dendritic atrophy in inferior colliculus neurons and did not affect neuronal morphology in the superior colliculus. Furthermore, stressed rats showed a stronger impairment in acoustic conditioning than in visual conditioning. Fifteen days post-stress the inferior colliculus neurons completely restored their dendritic structure, showing a high level of neural plasticity that is correlated with an improvement in acoustic learning. These results suggest that chronic stress has more deleterious effects in the subcortical auditory system than in the visual system and may affect the aversive system and fear-like behaviors. Our study opens a new approach to understand the pathophysiology of stress and stress-related disorders such as major depression.

Acceleration of vertical migration of corneal epithelial cells in albino rats during chronic immobilization stress

This paper studies the effect of chronic immobilization stress on the kinetics of corneal epithelial cells from the basal layer into higher layers. Experiments were carried out on 49 male rats. The animals were given an intraperitoneal injection of tritium-thymidine and an additional application of 5 microCi of tritium-thymidine was made to its surface because the cornea has no blood supply. The animals were killed and the cornea removed for investigation. Values of the index of labeled nuclei and intensity of thymidine labeling, characterizing DNA synthesis in the corneas of the control and experimental animals showed no significant change compared with their values in a pervious series of experiments. Chronic exposure to stress increased the velocity of vertical migration of the cells from the basal layer toward the outer layers of the cornea.

Effect of Chronic Immobilization Stress on Tissue Distribution of Vitamin A in Rats Fed a Diet with Adequate Vitamin A

The effect of consecutive daily immobilization stress on the metabolism of vitamin A was studied in rats by following changes in tissue distribution of the vitamin for 14 days. Male rats, fed a diet with adequate vitamin A, were subjected to 4 hours of daily immobilization for 1, 3, 7, 10 or 14 days. Ponderal growth was completely abolished, and serum vitamin A fell markedly. The amount of vitamin A in liver, testes and kidney decreased after the first period of restraint. On the other hand, the amount of vitamin A in adrenal glands increased gradually and reached a maximum (+62.3%) on the 7th day. In conclusion, this experiment showed that daily intermittent immobilization provoked a marked change in distribution of vitamin A in tissues.immobilization stress vitamin A distribution