جستجوی مقالات مرتبط با کلیدواژه « Restraint stress » در نشریات گروه « پزشکی »

The efficacy of escitalopram, a pharmaceutical antidepressant, and exercise, a lifestyle intervention, in mitigating depressive symptoms has been established. This study investigated the impact of varying doses of escitalopram and the combination of forced exercise with escitalopram on stress-induced depressive-like behavior in male rats.

 Sixty-four male rats were allocated into eight groups: control (Co), sham (Sh), depression without treatment (Dep-WT), depression with exercise (Dep-Exe), depression with escitalopram at 10 mg/kg (Dep-Esc10), depression with escitalopram at 20 mg/kg (Dep-Esc20), depression with escitalopram at 10 mg/kg combined with exercise (Dep-Esc10-Exe), and depression with escitalopram at 20 mg/kg combined with exercise (Dep-Esc20-Exe). To induce depression, chronic restraint stress was administered for 6 hours per day over a period of 14 days.Following the stress induction period, rats were administered escitalopram (at doses of 10 or 20 mg/kg, i.p), subjected to treadmill running (20-21 m/min for 1 h/day), or subjected to a combination of both interventions. Depressive-like behaviour induced by stress and locomotor activity were assessed using the forced swimming test (FST) and the open field test (OFT), respectively.

 In the FST, the immobility time significantly increased in the Dep-WT, Dep-Exe, and Dep-Esc10 groups, while it significantly decreased in the Dep-Esc20, Dep-Esc10-Exe, and Dep-Esc20-Exe groups compared to the Dep-WT group. In the OFT, the central time and total travelled distance significantly decreased in the Dep-WT group. Conversely, central time significantly increased in the Dep-Esc10-Exe and Dep-Esc20-Exe groups, and all treatment groups exhibited a significant increase in central time compared to the Dep-WT group.

The findings suggest that combining exercise with escitalopram yields additive effects, representing a promising treatment protocol for anxiety, depression, and locomotor activity.

Chronic stress is related to cognitive impairment. Azadirachta indica A. Juss. (A. indica) leaf extract possesses antioxidant and cognitive enhancement effects. Therefore, this study was set up to evaluate the cognitive-enhancing effects of A. indica flower extract in stressed rats.

Male Wistar rats were randomly divided into control and stress groups. Restraint stress was induced to stress groups 3 h daily. The stressed rats were given vehicles, donepezil (a positive control meditation used to improve cognition), and A. indica at 250, 500, and 1000 mg/kg BW for 30 days. The novel object recognition test (NORT) was used to assess cognitive function, and the open field test (OFT) was utilized to assess spontaneous locomotor activity. Their brains and blood were taken to measure levels of brain-derived neurotrophic factor (BDNF), blood cortisol levels, and the density of survival neurons.

The discrimination index ratio of the stressed rats treated with either donepezil or A. indica flower extract at all doses was significantly improved as measured by NORT. Moreover, there was no significant difference between the control and stress groups in the locomotor behaviors of rearing and number of crossing. The stressed rats treated with donepezil and A. indica flower extract had significantly higher BDNF levels and also survival neuron density in the brain. However, their blood cortisol levels were lower than the stressed rats given the vehicle.

A. indica flower extract helps improve cognitive function in stressed rats by boosting BDNF and protecting against neuronal loss in the brain.

 Chronic stress exerts negative effects on cognitive functions through inducing changes in the hippocampus. Brain-derived neurotrophic factor (BDNF) is an essential factor in cognitive activities, which is considerably reduced under chronic stress. 1,25(OH)2 vitamin D plays neuroprotective roles partially by regulating the expression of various neurotrophic factors.

 Since few studies have studied the impact of vitamin D on BDNF level, we conducted this brief experiment to understand the role of vitamin D in maintaining hippocampal BDNF protein levels by using restraint as a model of chronic stress in rats.

 Rats underwent restraint stress 3 h/day for 28 days, during which they received vitamin D (5, 10 μg/kg) or its vehicle (IP, twice weekly). After the stress period, serum corticosterone (CORT) and hippocampus BDNF protein levels were measured.

 Restraint stress increased serum CORT (P < 0.001) and reduced BDNF protein levels (P < 0.001) as compared to the non-stress group. Vitamin D markedly maintained BDNF level close to normal (P < 0.001), but did not change CORT level significantly.

 This study demonstrated that 3h/day of chronic restraint stress for 28 days boosted serum CORT and declined hippocampal BDNF levels, similar to stronger restraint stress models. Vitamin D maintained BDNF level close to normal in the hippocampus, but it did not affect CORT level significantly.

Chronic stress impairs memory and certain brain functions such as locomotor activity. Crocin is one of the active components of saffron and has neuroprotective effects on brain functions. This study investigated crocin effects on locomotor activity and recognition of new conditions (exploration time) as well as novel object recognition and object location memories in chronic restraint stress rats.

Thirty-two male Wistar rats were randomly allocated to control group, restraint stress group (6h/day for 21days) and two groups receiving daily intraperitoneal injections of crocin (30 and 60mg/kg) accompanied by restraint stress. Memories were evaluated using the relevant novel object recognition (NOR) and object location (OLT) tests.

The NOR and OLT results, respectively, revealed significant and non-significant decreases in locomotor activity in the stressed group. The NOR results revealed enhanced locomotor activity due to crocin administration (30 and 60mg/kg). The NOR revealed significant enhancements in recognizing new conditions in both crocin treatments while the OLT test did so only with a crocin dose of 60mg/kg. Restraint stress and crocin treatments led to no significant differences in novel object recognition and object location memories. Finally, the stressed group exhibited significant increases in serum corticosterone levels but corticosterone levels declined significantly with crocin dose of 30mg/kg.

The high and low doses of crocin had different effects on the NOR and OLT variables under restraint stress conditions. The NOR test as cognitive test was found more sensitive to crocin treatments than the OLT test as spatial test although neither the memories showed changes in response to such treatment.

Physical exercise has positive effects on stress-induced pain response, while chronic stress persuades a negative effect on cognitive functions. Depending on the nature, duration and intensity of the stressor, it can repress pain (stress-induced analgesia) or exacerbate pain (stress-induced hyperalgesia). Furthermore, beneficial effects of Harmane on stress processes have been reported in rodents. This study aimed to investigate the effects of Harmane and moderate physical activity (associated or not) on pain response in restraint stressed mice.

Harmane was injected intraperitoneally at doses of 0.1, 0.3 and 0.6 mg/kg, every other day until 28 days, and pain response of the adult NMRI mice was detected using the hot-plate test

The results exhibited that Harmane, at all doses used, did not alter pain perception in mice; however, 3- but not 6 and 9-day restraint stress (3 hours per day) induced hyperalgesia per se. In addition, Harmane reduced hyperalgesia in 3-day stressed mice, while moderate treadmill running (10 m/min for 30 min/day, 5 day/week) caused hyperalgesia in 6- and 9-day stressed mice. Furthermore, the hyperalgesia induced by moderate treadmill running in 9-day stressed mice restored by Harmane.

The findings indicated that Harmane has a protective effect on hyperalgesia induced by stress per se or potentiated effect of moderate treadmill running in stressed mice.

Lead is known as an environmental contaminant with neurotoxic properties. In addition, people experience different types of chronic stress, especially in developing countries. It has been established that lead   or stress causes structural and physiological damages to the neural pathway like dopaminergic connections. Nevertheless, the effect of lead and restraint stress on movement behaviors when are experienced together has not been studied yet. In this study, male albino mice were randomly divided into different groups (n = 6). Lead acetate was daily injected at 15 mg/kg intraperitoneally for 2, 4, or 6 weeks. Restraint stress  (6 h in a day) was applied alone or in combination with lead acetate for 2, 4, or 6 weeks. The catalepsy, akinesia, and the balance of animals were measured by bar test, elevated beam device, and rotarod to evaluate the movement disorders. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, a known neurotoxin causes movement disorders, was used as positive control group. The results showed that exposure to the lead or stress or their combination for 6 weeks caused catalepsy, akinesia, and imbalance in the animals,while exposure for 2 or 4 weeks didn’t affect the movement items indices. The combination of leadand stress did not show any significant difference compared to the exposure to each of them individually.  From the findings, Lead, stress, and their combination caused movement disorders in a time dependent manner. Short time exposure did not change movement behavior. The co-exposure to the lead and stressdid not show additive or synergistic effects.

There are limited numbers of experimental studies related to the potential role of parathormone/parathyroid hormone (PTH) in response to psychological stress. In the current study, we aimed to cross-examine, for the first time, changes in PTH plasma concentration and the expression of its molecular targets mediated by restraint stress in rats. Male Wistar rats (n = 42) were separated into control and stressed groups. They were further divided into two groups that received chronic restraint stress (CRS) for 7 and 28 consecutive days (n = 7 for each group). Elevated plus maze and tail suspension test were used to determine the anxiety- and depressive-like behaviors of a different set of rats including stress and control groups (n = 7 for each group). The plasma levels of adrenocorticotropic hormone (ACTH), corticosterone, and intact parathormone (iPTH) were measured by enzyme-linked immunosorbent assay (ELISA). In addition, alterations in the expressions of glucocorticoid receptor (GR), calcium sensing receptor (CaSR), and parathormone receptor (PTHR1) of kidney and total thyroid gland tissues were estimated by Western Blotting. There was no significant difference in the plasma level of iPTH while significant increases in the levels of ACTH and corticosterone were noted in the stressed-animals at day 7 and 21 (P = 0.010 and P = 0.016, respectively) of restraint stress. However, we found a negative correlation between iPTH and corticosterone levels in acute restraint stress (r = 0.771, P = 0.002). In addition, the expression of PTHR1 significantly decreased in the kidney at day 7 (P = 0.001) and in the thyroid gland at day 28 (P = 0.05) in response to CRS. To sum up, CRS has a significant effect on the expression of parathormone receptor rather than the iPTH concentration. The present results add a new dimension to stress research through the negative effect of chronic stress on the PTH signaling pathway.

Stressful events during gestation have important effects on the later physical and mental health of the offspring. The present study aimed to identify effects of co-administration of stress and morphine in prenatal period and re-exposure to stress at the end of infancy on corticosterone blood levels and pentylentetrazol-induced epileptic behaviors in rat.

Pregnant rats were divided to six groups of control, stress, saline, morphine, stress-saline and stress-morphine. In the stressed group, rats were stressed and held immobile for three consecutive days started on day 15 of pregnancy. The rats in saline and morphine groups received saline and morphine in the same days. In the morphine/saline-stress groups, rats were exposed to stress and received morphine/saline simultaneously. On postnatal day 22, half of the pups re-exposed to stress, and pentylentetrazol-induced epileptic behaviors of each rat were assessed. Blood samples were collected to determine corticosterone level.

Latency of first epileptic behavior decreased significantly in stress-morphine group compared to other groups. Re-exposure to stress significantly led to a decrease in number of clonic seizure. There was no significant difference between the experimental groups in duration of clonic attacks and mortality rate. The level of corticosterone showed a significant increase in stressed pups and decreased in morphine group.

these results indicated that co-administration of morphine and restraint stress during late pregnancy had profound impact on neurochemical development and might alter vulnerability to PTZ-induced epileptic behaviors. Prenatal stress is more powerful than postnatal stress on influencing neural development and seizure susceptibility in rats.

Cholecystokinin (CCK), a peptide hormone found in the gut is the most abundant peptide neurotransmitter in the brain as well, and its effects on learning, memory, and anxiety have been shown. However, it is not clear whether this substance acts as a mediator for anxiety and stress induction or inhibits them. Hence, the purpose of this study was to evaluate the effects of CCK on memory function under stress conditions.

Male Wistar rats were divided into four groups: The control, the control‑CCK, the stress, and stress‑CCK. To induce stress, the rats were placed within adjustable restraint chambers for 6 h daily, for 24 days. CCK‑8S (cholecystokinin sulfated octapeptide was injected before induction of stress (1.6 µg/kg, intraperitoneal) for 24 days. Passive avoidance learning test was used for evaluation of learning and memory. Rats received foot electrical shock before stress induction and CCK injection and step through latencies were evaluated 1‑day after the last session of stress and treatments.

Stress impaired memory significantly (P < 0.05). Although CCK per se decreased memory (P < 0.05), it prevented the memory impairments in the stress group as there was no significant difference between the control and stress‑CCK groups.

Stress has a profound effect on cognition and CCK probably acts as a mediator for its action. Our results showed that a high concentration of CCK during stress may be helpful in alleviating the effects of stress on the brain.