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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although final brain size and the number of available neurons and axons appear to be established early in infancy, plasticity of the brain continues during adolescence through an integrated process of overproduction and elimination of synapses and receptors. In addition, hormonal levels change dramatically during this period, as a result of the onset of puberty. This age-specific condition has been suggested to serve as a permissive factor for the emergence of a number of early-onset neuropsychiatric disorders, including schizophrenia, attention-deficit hyperactivity disorder (ADHD), and perhaps substance abuse. However, relatively few investigations have focused on animal models of this developmental phase. The periadolescent rodent (similar30-45-day-old), has been proposed as a useful model. Periadolescent rats and mice are generally associated with a peculiar behavioral profile, consisting of basal hyperactivity, high attraction towards novel stimuli and a marked involvement in affiliative and playful behaviors. Moreover, a unique profile of psychopharmacological responsivity characterizes rodents around this age. Recent experiments by our group investigated age-related discontinuities in the response of the hypothalamic-pituitary-adrenal axis (HPA) to both stress and psychostimulants. The latter are often administered as therapeutic drugs to children with ADHD, which have been also associated with an impaired response to stress and abnormalities in HPA axis function. Indeed, an altered functioning of the HPA axis has been proposed as a possible risk factor and a potential marker for such a behavioral vulnerability. Animals were studied at adulthood (> pnd 70) or during periadolescence. Experiment I characterized basal corticosterone (CORT) levels in naive mice kept undisturbed in standard social conditions from weaning to sacrifice. Periadolescent male mice showed higher basal CORT levels than adult subjects, suggesting that the set up of the HPA axis is physiologically elevated during adolescence. In experiment II, we investigated age-related differences in the response to both acute and chronic stress conditions. Periadolescent and adult mice were housed either in a standard (three animals per cage) or in a crowding condition (nine animals per cage). The latter has been indeed reported to potentiate the subsequent reaction to acute stress in adult rodents. At the end of this period and following 24 h individual housing, mice were injected with either saline (SAL) or a standard amphetamine (AMPH) dose (2 mg/kg), and faced with a mild acute psychological stress, namely removal of sawdust from the home cage. Important sex differences emerged in animals of the two ages. Periadolescent females showed a reduced CORT response to acute stress. Within the adult male group, the chronic crowding condition produced a prominent potentiation of CORT response to the acute stress challenge. Conversely, this profile was not evidenced in periadolescents. These results indicate a strong role for gender and social variables in the response of periadolescent subjects to the various aspects of stress. As for AMPH effects, in the absence of significant changes in adult subjects, the drug produced a marked CORT release in periadolescent mice. A better understanding of neuroendocrine-related AMPH effects as a function of social and environmental risk factors during adolescence, might deepen our knowledge on the neurobiological bases of genetically determined neuropsichiatric disorders and possibly improve the therapeutical efficacy of psychostimulant drugs.
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PMID:Peculiar response of adolescent mice to acute and chronic stress and to amphetamine: evidence of sex differences. 1186 27

To determine whether docosahexaenoic acid (DHA) affects stress responses in rats, we investigated its influence on several behavioral tests. Female rats were fed a diet deficient in (n-3) fatty acid from mating through pregnancy and lactation. Male pups fed the same diet as their dams were used for experiments. The effects of dietary (n-3) fatty acid deficiency and supplementation with DHA on psychological stress and conditioned-fear stress were investigated. The effect of DHA on psychological stress was examined by an elevated plus-maze test. The (n-3) deficient rats spent significantly (P<0.05) less time in the open arms; after 1 week of supplementation with DHA, they showed a significant (P<0.01) improvement. We then examined the paired effects of DHA and CRH on stress manifestations by an intracerebroventricular (i.c.v.) cannulation and behavior testing. An i.c.v. infusion of CRH (500 pmol) under resting conditions was shown to have stress-inducing effects on behavior such as decreases of rearing, smelling and feeding, and increases of face washing; the supplementation of DHA significantly improved these distress behaviors. Finally, conditioned fear was induced by 40 min forced exposure to a cage in which the rat had experienced footshocks (30 x 1 mA x 1 s) 1 day before. Freezing behavior was dramatically suppressed by the supplementation of DHA, even 48 h after the conditioning treatment. Furthermore, the effect of DHA on the conditioned fear stress response is maintained over a long-term period. The i.c.v. pre-treatment of rats with bicuculline, a GABA(A) receptor antagonist, enhanced the conditioned-fear-induced freezing time in a dose-dependent fashion in the (n-3) fatty acid deficient animals. Significantly, the DHA supplemented group was not affected by the pre-treatment with bicuculline. From these findings, it is concluded that the involvement of DHA in stress responses may act via a GABA(A) receptor-mediated mechanism.
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PMID:Possible regulatory mechanism of DHA-induced anti-stress reaction in rats. 1257 22

Social isolation and lack of social support have deleterious effects on health, thus being regarded as one of the most relevant causes of diseases in human and other mammalian species. However, only few are the studies aimed at evaluating the psychoneuroimmunological functions of individually housed subjects. The present study was designed to understand how the behavior and the physiology of male house mice might be affected by individual housing. We first analyzed whether individual housing of different duration (1-42 days) would result in immuno-endocrine dysfunction (experiment 1). Then we investigated whether housing conditions would affect the reaction to an acute mild psychological stress (experiments 2 and 3). There were three main findings: first, individually housing mice for increasing time periods did not induce any major immuno-endocrine effects compared to a stable sibling group housing. Therefore, prolonged isolation does not seem to dramatically impair mice immuno-endocrine functions. Second, when exposed to a mild acute stress, i.e. forced exposure to a novel environment, isolated mice showed higher basal corticosterone and lower type 1 (IL-2) and type 2 (IL-4) cytokines as well as splenocytes proliferation compared to group housed male mice. Finally, when faced with a free choice between a novel environment and their home cage, individually housed mice showed reduced neophobic responses resulting in increased exploration of the novel environment, thus suggesting a low anxiety profile. Altogether, our findings suggest that individual housing in itself does not change immunocompetence and corticosterone level, but does affect reactivity to a stressor. In fact, individually housed mice showed high behavioral arousal, as well as altered immuno-endocrine parameters, when challenged with mild psychological novelty-stress.
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PMID:Individual housing induces altered immuno-endocrine responses to psychological stress in male mice. 1268 11

Previous studies have disagreed about whether prostaglandin EP1 or EP3 receptors are critical for producing febrile responses. We therefore injected lipopolysaccharide (LPS) at a variety doses (1 microg kg(-1)-1 mg kg(-1)) intraperitoneally (i.p.) into wild-type (WT) mice and mice lacking the EP1 or the EP3 receptors and measured changes in core temperature (Tc) by using telemetry. In WT mice, i.p. injection of LPS at 10 microg kg(-1) increased Tc about 1 degrees C, peaking 2 h after injection. At 100 microg kg(-1), LPS increased Tc, peaking 5-8 h after injection. LPS at 1 mg kg(-1) decreased Tc, reaching a nadir at 5-8 h after injection. In EP1 receptor knockout (KO) mice injected with 10 microg kg(-1) LPS, only the initial (< 40 min) increase in Tc was lacking; with 100 microg kg(-1) LPS the mice showed no febrile response. In EP3 receptor KO mice, LPS decreased Tc in a dose- and time-dependent manner. Furthermore, in EP3 receptor KO mice subcutaneous injection of turpentine did not induce fever. Both EP1 and EP3 receptor KO mice showed a normal circadian cycle of Tc and brief hyperthermia following psychological stress (cage-exchange stress and buddy-removal stress). The present study suggests that both the EP1 and the EP3 receptors play a role in fever induced by systemic inflammation but neither EP receptor is involved in the circadian rise in Tc or psychological stress-induced hyperthermia in mice.
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PMID:Characteristics of thermoregulatory and febrile responses in mice deficient in prostaglandin EP1 and EP3 receptors. 1283 30

We assessed the hypothesis that chronic estrogen replacement in ovariectomized rats has the beneficial effect of suppressing stress-induced cardiovascular responses through endothelial nitric oxide synthase (eNOS). We employed a radiotelemetry system to measure blood pressure and heart rate (HR). Female Wistar rats aged 11 wk were ovariectomized and implanted with radiotelemetry devices. After 4 wk, the rats were assigned either to a placebo-treated group (Placebo; n=6) or a group treated with 17beta-estradiol (Estrogen; n=8) subcutaneously implanted with either placebo- or 17beta-estradiol (1.5 mg/60-day release) pellets under anesthesia. These rats underwent either of the two types of stress after 4 wk of estrogen or placebo treatment. Cage-switch stress and restraint stress rapidly and continuously elevated the mean arterial pressure (MAP) and HR both in the Placebo and Estrogen groups. However, the MAP and HR responses to cage-switch stress and the MAP but not HR response to restraint stress were attenuated significantly in the Estrogen group compared with the Placebo group. A NOS inhibitor, NG-nitro-L-arginine methyl ester, given in drinking water, reduced the difference in the pressor response to cage-switch between the Estrogen and Placebo groups. In addition, Western blot analysis showed that eNOS expression in the mesentery was increased in the Estrogen group compared with the Placebo group. Thus for the first time we showed that mesenteric eNOS overexpression could explain at least partly why chronic estrogen treatment suppressed the enhanced cardiovascular responses to psychological stress in the ovariectomized rat.
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PMID:Estrogen replacement suppresses stress-induced cardiovascular responses in ovariectomized rats. 1523 1

There are lines of evidence that natural killer (NK) cells are sensitive to physical and psychological stress. Alterations in the immune system including NK cells are known to differ among tissues and organs. The effect of stress on the lung immune system, however, has not been well documented in spite of the fact that the lungs always confront viral or bacterial attacks as well as tumour cell metastasis. In this study, we intended to investigate the effect of restraint stress on lung lymphocytes including NK cells. C57BL/6 mice were exposed to 2 h restraint stress. The concentration of plasma epinephrine significantly rose immediately after the release from restraint as compared to home-cage control mice. Flow cytometric analysis revealed that the numbers of most lymphocyte subsets including NK cells were decreased in the lungs and blood but not in the spleen, immediately after restraint stress. Immunohistochemical examination revealed that the number of NK cells was decreased in the intraparenchymal region of the lungs, while the number of alveolar macrophages did not change. The decrease in the number of NK cells in the lungs and blood was reversed by the administration of propranolol, a nonselective beta adrenergic antagonist. Taken together, our findings suggest that acute stress reduces the number of intraparenchymal lung NK cells via activation of beta adrenergic receptors.
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PMID:Acute stress reduces intraparenchymal lung natural killer cells via beta-adrenergic stimulation. 1560 10

The ability to mount a successful response to threats is critical for an organism's survival. A key element of the stress response is its nonspecificity toward the stress source, with similar endocrine and behavioral changes expected under a variety of stressors. In this project we utilized an experimental design that accounts for multiple sources of variation to further understand the nature of stress responsivity and its relationship to the early rearing environment. A sample of baboons (n=73) was observed during the early phase of life in their social group, and then tested as juveniles in a challenging situation. Maternal cortisol levels were measured during the peripartum period. The challenging situation (individuals were isolated for a few minutes in a single cage) was designed to be a moderate source of psychological stress. Patterns in individual differences during the stress test were "mapped" by means of multidimensional scaling (MDS). After the observation was made, the subject was sedated and a blood sample was taken to measure cortisol levels. Our results indicate that when juvenile baboons are confronted with a source of psychological stress, they show a multidimensional behavioral response, probably mediated by the activation and synergic interaction among different neurohormonal systems that, ultimately, act on the hypothalamus-pituitary-adrenal (HPA) axis. Different components of the multidimensional, or nonspecific, behavioral response are associated with the quality and quantity of interactions with their mothers during early life. Juveniles whose mothers displayed higher levels of positive interaction were characterized by vigilant but less active reactions to the stress test, whereas juveniles of mothers that displayed high levels of stress-related behaviors had higher cortisol and locomotion levels.
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PMID:Maternal care and development of stress responses in baboons. 1601 61

Psychological stress elevates blood pressure through sympathetic nerve activation. This pressor response is supposedly associated with cardiovascular events. We investigated a sex difference in the pressor response and norepinephrine surge to cage-switch stress in rats. Wistar male and female rats were catheterized for blood pressure monitoring and blood sampling. Six days post-surgery, the rats were exposed to the cage-switch stress and blood samples were collected at rest and 30 min after the start of the stress. The stress-induced pressor response was greater in the male than in the female rats. The stress significantly increased the norepinephrine level in the male, but not in the female rats. Pre-treatment with N(G)-nitro-l-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, attenuated the norepinephrine response significantly in the male rats. There was no sex difference in the endothelial NO synthase expression in the gastrocnemius muscle. However the phosphorylation at serine 1177, a marker for eNOS activation, was higher in the male than in the female rats. These results suggest that NO is involved in the norepinephrine surge to psychological stress in the male rats, but not in the female rats. This is the first report on a sex difference in the norepinephrine surge in response to psychological stress through NO, in association with pressor response.
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PMID:Sex difference in norepinephrine surge in response to psychological stress through nitric oxide in rats. 1717 36

Although increases in glucocorticoid concentrations during acute stress are believed to help animals survive stressful events, chronic changes in glucocorticoid concentrations can alter metabolism and lead to disease. We studied the effect of chronic psychological stress on corticosterone (CORT), corticosterone binding globulin (CBG), glucose, and triglyceride concentrations as well as immune responsiveness to a T-cell mitogen challenge in European starlings, Sturnus vulgaris. To induce chronic stress we used a chronic stress protocol consisting of five stressors (loud radio, cage tapping, cage rolling, human voice, and bag restraint) administered in random order for 30 min for 4 times/day over 18 days. Total CORT decreased throughout the chronic stress period, which parallels a previous study with starlings. CBG capacity did not significantly change with chronic stress, thus free CORT followed the same pattern of attenuation as total CORT during chronic stress. Despite the change in regulation of CORT release, daytime glucose and triglyceride concentrations did not change with chronic stress. In addition, immune responsiveness in chronically stressed and unstressed birds was similar. Our results, together with a previous study using a similar CSP in European starlings, suggest that starlings physiologically dampen the HPA axis during chronic psychological stress to avoid pathology associated with chronically augmented CORT concentrations such as hyperglycemia and impaired immune function.
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PMID:The effect of chronic psychological stress on corticosterone, plasma metabolites, and immune responsiveness in European starlings. 1768 4

In the hippocampus, a brain structure critically important in the stress response, GABA controls neuronal activity not only via synaptic inhibition, but also via tonic inhibition through stimulation of extrasynaptic GABA receptors. The extracellular level of GABA may represent a major determinant for tonic inhibition and, therefore, it is surprising that its responsiveness to stress has hardly been investigated. To clarify whether hippocampal extracellular GABA levels change in response to acute stress, we conducted an in vivo microdialysis study in rats. We found that dialysate GABA levels respond to various neuropharmacological manipulations such as reuptake inhibition, elevated concentrations of K(+), tetrodotoxin and baclofen, indicating that a large proportion of hippocampal extracellular GABA depends on neuronal release and that GABA re-uptake plays a role in determining the extracellular levels of this neurotransmitter. Next, rats were exposed to a novel cage or to forced swimming in 25 degrees C water. Interestingly, these two stressors resulted in opposite effects. Novelty caused a fast increase in GABA (120% of baseline), whereas forced swimming resulted in a profound decrease (70% of baseline). To discriminate between the psychological and physical aspects (i.e. the effects on body temperature) of forced swimming, another group of animals was forced to swim at 35 degrees C. This stressor, like novelty, caused an increase in hippocampal GABA, suggesting a stimulatory effect of psychological stress. The effects of novelty could not be blocked by the corticotropin-releasing factor receptor antagonist D-Phe-CRF(12-41). These results are the first to demonstrate stressor-dependent changes in hippocampal extracellular GABA; an observation which may be of particular significance for GABAergic tonic inhibition of hippocampal neurons.
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PMID:Exposure to novelty and forced swimming evoke stressor-dependent changes in extracellular GABA in the rat hippocampus. 1769 36


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