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

Glucocorticoids modulate brain function and behaviour through different mechanisms. Although classical effects are mediated through intracellular receptors that modulate gene transcription, recent evidence supports the existence of rapid, nongenomic steroid effects through the neuronal membrane. In this study, we explored possible rapid behavioural effects of corticosterone in the rat, which could provide a model to characterize further the mechanisms involved in rapid corticosteroid nongenomic actions. We found that a corticosterone injection, at doses (2.5 or 5 mg/kg) that mimic plasma concentrations produced by substantial stress, rapidly increases (within 7.5 min of its systemic administration) the locomotor response displayed by rats in a novel environment (activity cage). A lower dose of 1 mg/kg failed to induce this effect. In addition, corticosterone failed to increase locomotion when administered to rats that had been previously exposed to the activity cage. Corticosterone-induced increased locomotion in a novelty situation was not counteracted by either the intracerebroventricular administration of the protein synthesis inhibitor cycloheximide, or by the intracerebroventricular administration of specific antagonists for each type of intracellular corticosteroid receptor, i.e. RU28318, a mineralocorticoid receptor antagonist and RU38486, a glucocorticoid receptor antagonist. Further studies supported the viability of the receptor antagonists to display an anti-corticosteroid action interfering, as previously reported, with the behavioural &winning test. Therefore, the rapid actions of corticosterone in locomotor activity described here, which appear to be nongenomic, might provide a model for future research on the elucidation of the mechanisms involved in steroid-membrane interactions.
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PMID:Novelty-related rapid locomotor effects of corticosterone in rats. 908 30

The aim of this study was to investigate the effect of training on the in vivo tibial structural strength during the development of post-ovariectomy osteoporosis. Seventeen mature Wistar rats (215 g) were ovariectomized and randomized into two groups. The sedentary control group was kept cage confined, while 3 days postoperatively the trained group started treadmill running with high intensity for 1 h 5 days a week. All were given a low calcium diet (Ca 0.01%). After 8 weeks the animals were anaesthetized and the right lower legs fractured during muscle contraction in three-point ventral bending. The left legs were fractured at the same level after removal of all soft tissues. Histomorphometry of the meta- and diaphysis of the distal tibiae was performed. Weight-gain was higher in sedentary (108 g) than in trained (61 g) rats (P<0.0001). There were no significant differences in mechanical results between the groups at in vivo or in vitro fracture. Correcting for weight-gain differences did not change these results. Histomorphometry showed no differences between the groups. Corticosterone was higher in trained than in sedentary rats (P<0.02), and corticosterone may have had a negative influence both on muscle and bone. The study could not show an effect of high intensity training in the early phase after ovariectomy on in vivo or in vitro fracture strength.
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PMID:Effect of intensive training on lower leg structural strength: an in vivo study in ovariectomized rats. 924 Oct 27

The purpose of the present study was to evaluate the role of central alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA)/kainate type of glutamate receptors in the control of ACTH and corticosterone release under basal and stress conditions. AMPA/ kainate competitive receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX), which does not penetrate the blood-brain barrier, was administered intracerebroventricularly (i.c.v.). A modified method for i.c.v. drug administration in conscious freely moving rats was employed. DNQX or artificial cerebrospinal fluid (aCSF) was injected into lateral ventricle through a thin polyethylene cannula with a steel needle on the end which was inserted and moved via large polyethylene cannula to the guide stainless steel cannula. This procedure was performed out of the cage. ACTH and corticosterone release under basal conditions and during immobilization stress were investigated. Intracerebroventricular administration of DNQX resulted in an increase of ACTH and corticosterone in plasma reaching maximal values at 15 min after drug injection. During immobilization stress, i.c.v. DNQX induced a mild reduction in plasma ACTH levels compared to those in aCSF pretreated rats. Corticosterone secretion was high throughout the whole period of stress exposure. These findings indicate that endogenous excitatory amino acids (EAA) acting at AMPA/kainate receptors may interfere with the control of ACTH release under both basal and stress conditions, but the mechanisms involved remain to be elucidated.
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PMID:Effect of central administration of the non-NMDA receptor antagonist DNQX on ACTH and corticosterone release before and during immobilization stress. 937 80

This work was developed during an investigation on the neuroendocrine-immune interaction in rats immune challenged with sheep red blood cells (SRBC). The structures used for evaluating the immunological response was the direct plaque-forming cells (PFC). An inbred strain of rat was used to overcome the problem of different timings in the peak humoral immune response. Normal rats were injected intraperitoneally with saline or SRBC and were killed 0, 3, 4, 5, and 6 days later. Body and gland weights were recorded, and. serum levels of corticosterone and prolactin were quantified by radioimmunoassay. The hormone levels and gland weights of the saline conspecifics and SRBC-treated rats were found to be similar. When new rats were housed in a separate room and treated with physiological saline, there were again no differences in the body and gland weights or the serum hormone levels between the two home cage control (HCC) groups of animals. Compared with saline conspecifics and SRBC-treated groups, the HCC groups had higher body weights from the third to the sixth day of treatment and had lower gland weights in absolute and relative analysis (pituitary, thyroid, and adrenals) mainly on the fourth and fifth days; thymus weights were highest on the third day. Corticosterone and prolactin levels were significantly lower on the fifth and sixth days, respectively. Because SRBC-treated rats showed a peak direct immune response on the fourth and fifth days and showed peak corticosterone levels on the fifth day after treatment, we conclude that the former animals were under stress and influenced their saline conspecifics through sound or smell. This conclusion agrees with other studies, showing that physically or emotionally stressed rats can influence conspecifics through noise and body odors.
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PMID:Immunological stress in rats induces bodily alterations in saline-treated conspecifics. 1086 87

Thousands of soldiers who served in the Gulf War have symptoms that have been collectively termed Gulf War Illness (GWI). It has been suggested that a combination of operational stress and pyridostigmine, a drug given as a pretreatment to protect soldiers against the effects of exposure to nerve agents, might have had unexpected adverse health effects causing these symptoms. Our laboratory has previously modeled operational stress in rats using a paradigm of around-the-clock intermittent signalled footshock. In the present studies, this model was used to investigate the potential synergistic effects of chronic stress and pyridostigmine on physiology and behavior. Seventy-two rats were trained to perform an alternation lever pressing task to earn their entire daily food intake. The rats were then implanted with osmotic minipumps containing vehicle, pyridostigmine (25 mg/ml pyridostigmine bromide) or physostigmine (20 mg/ml eserine hemisulfate). The pumps delivered 1 microl/h, which resulted in a cumulative dosing of approximately 1.5 mg/kg/day of pyridostigmine or 1.2 mg/kg/day of physostigmine, equimolar doses of the two drugs. The rats were then returned to their home cages where performance continued to be measured 24 h/day. After 4 days, 24 of the 72 rats were trained to escape signalled footshock (avoidance-escape group) and 24 other rats (yoked-stressed group) were each paired to a rat in the avoidance-escape group. The remaining 24 rats were not subjected to footshock (unstressed group). Shock trials were intermittently presented in the home cage 24 h/day for 3 days, while alternation performance continued to be measured. Since only 12 test cages were available, each condition was repeated to achieve a final n of six rats per group. Pyridostigmine and physostigmine each decreased blood acetylcholinesterase levels by approximately 50%. Physostigmine also decreased brain cortical acetylcholinesterase levels by approximately 50%, while pyridostigmine had no effect on cortical acetylcholinesterase activity. Alternation performance was impaired on the first day of stress and then recovered. Neither pyridostigmine nor physostigmine affected performance in the absence of stress or increased the effects of stress alone. Corticosterone was significantly increased in the yoked stress group compared to unstressed controls. These data suggest that pyridostigmine does not exacerbate the effects of stress on performance or levels of stress hormones. Furthermore, these data do not suggest that stress enables pyridostigmine to cross the blood brain barrier.
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PMID:The combined effects of pyridostigmine and chronic stress on brain cortical and blood acetylcholinesterase, corticosterone, prolactin and alternation performance in rats. 1170 Nov 90

Brain alpha(1)-adrenoceptors are known to be necessary for motor activity in rodents and have been shown to be altered by stress and corticosteroids but only in biochemical experiments. To determine if the behaviorally coupled receptors are also affected by stress, the present study examined the effect of stress and corticosteroids treatment on the motor activity response to modafinil, a putative alpha(1)-adrenoceptor agonist, which is unique in that it elicits extremely high levels of activity via these receptors. Mice were subjected to various schedules of restraint stress for 1-6 days and were subsequently tested for either modafinil-induced or dopaminergically induced behavioral activity in the home cage using videotape recording. In experiments on corticosteroid treatment, mice received exogenous corticosterone or dexamethasone in the drinking water before and during the stress and were tested for modafinil-induced activity as above. It was found that the stress significantly reduced the response to the drug by the third daily session. Motor responses to dopaminergic agents including apomorphine, amphetamine, dihydrexidine and quinpirole were either not altered or were increased at this time. Treatment of animals with corticosterone or dexamethasone prior to and during stress prevented the behavioral subsensitivity to modafinil. Corticosterone pretreatment markedly suppressed the plasma corticosterone response to the stress. The present results provide further support for the hypothesis that stress produces a selective desensitization or inhibition of motor-related brain alpha(1)-adrenoceptors and that this effect can be prevented by corticosteroid treatment.
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PMID:Stress-induced subsensitivity to modafinil and its prevention by corticosteroids. 1221 44

Administration of bacterial endotoxin (lipopolysachharide; LPS) elevates proinflammatory cytokines, such as interleukin-1beta (IL-1beta) and IL-6, and activates the hypothalamic-pituitary-adrenal (HPA) axis. Corticosterone (CORT), the glucocorticoid (GC) effector hormone of the HPA axis in rats, inhibits both proinflammatory cytokine production/release and activity of the HPA axis itself. Exposure to chronic or repeated stressors often induces resistance to the effects of GCs. The following experiments were conducted to test the hypothesis that an acute stressor, inescapable tailshock (IS), alters responsivity of the HPA axis and proinflammatory cytokine system to dexamethasone (DEX), a synthetic GC. First, we examined the ability of various doses of DEX to suppress proinflammatory cytokine and HPA activity in response to LPS challenge 24 h after either home cage (HCC) or IS treatment. Upon finding resistance to DEX in IS animals, we examined the duration of the altered response to DEX by testing animals 1, 4 and 21 days after IS. To test whether IS animals were selectively resistant to the suppressive effects of DEX on the response to LPS, the ability of DEX to suppress HPA activity in response to a non-inflammatory stressor, exposure to an elevated "pedestal", was assessed. Again, DEX resistance was observed in IS animals. Finally, we examined whether changes in the responsivity to DEX were dependent upon the controllability of the stressor. The induction of DEX resistance was independent of the degree of behavioral control that the animal had over the stressor. Thus, a single session of IS induces DEX resistance of both HPA axis and cytokine responses measured in vivo.
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PMID:Inescapable shock induces resistance to the effects of dexamethasone. 1268 7

Sleep deprivation is associated with cocaine-enhanced genital reflexes in male rats, and castration of the male rat causes a decline in sexual behaviour, which can be reversed by hormone administration. We conducted two experiments to determine whether sleep deprivation and cocaine administration could also induce spontaneous penile erection in castrated rats after hormonal treatment (testosterone, progesterone and oestradiol). Different doses of hormones or vehicle were administered to rats during the 4-day period of sleep deprivation, and in home-cage control rats. Testosterone did not restore penile erection in castrated sleep-deprived rats. Progesterone triggered penile erection, and 100 mg/day of progesterone induced the highest proportion of rats displaying penile erection, and restored the frequency of penile erection observed in noncastrated sleep deprived rats. Penile erection was absent in vehicle as well as oestradiol-treated sleep-deprived castrated rats. Whereas sleep deprivation increased progesterone concentrations in noncastrated rats, sleep deprivation decreased progesterone concentrations in castrated rats. Corticosterone concentrations were lower in the castrated sleep-deprived rats than in respective control group. These data show that progesterone treatment facilitates penile erection in sleep deprived-cocaine castrated rats.
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PMID:Hormone treatment facilitates penile erection in castrated rats after sleep deprivation and cocaine. 1476 2

Behavioral, hormonal and neuronal responses to prolonged exposure to the volatile components of essential oil (EO) extracted from citrus lemon were investigated in male and female rats. Animals were exposed to the lemon essence for 2 weeks while in their cage. Anxiety was then determined with the elevated plus-maze apparatus while nociception was evaluated with a phasic thermal pain stimulus (plantar test) and with a chemical pain stimulus (formalin test). At the end of the experimental sessions, brain areas were dissected to measure beta-endorphin (beta-EP) concentrations in the hypothalamus and periaqueductal gray matter (PAG). Blood samples were collected to determine corticosterone plasma levels. In both sexes, prolonged EO exposure decreased the time spent in the open arms of the plus-maze apparatus. EO-exposed males and females showed higher thermal nociceptive thresholds than controls when tested with the plantar test apparatus. EO exposure induced female-specific decreases in formalin-induced pain behaviors during the formalin test. beta-EP concentrations in the hypothalamus and PAG were affected by EO. Corticosterone was lower in EO-exposed animals of both sexes than in their controls. These results suggest that long-term exposure to lemon EO can induce significant, at times sex-specific, changes in neuronal circuits involved in anxiety and pain.
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PMID:Effects of long-term exposure of lemon essential oil odor on behavioral, hormonal and neuronal parameters in male and female rats. 1497 56

The hormonal response to stress is enhanced by oestrogen but inhibited by androgens. To determine underlying changes in activity of neuropeptide neurones in the paraventricular nucleus of the hypothalamus (PVN), we examined the effect of oestrogen and androgen treatment on restraint-induced c-fos mRNA, corticotropin-releasing hormone (CRH) heteronuclear RNA, and arginine vasopressin hnRNA expression in the PVN. Male rats were gonadectomized and injected with oestradiol benzoate (EB) or dihydrotestosterone propionate (DHTP; s.c., daily for 4 days). Rats were stressed by restraint for 10 min or 30 min before killing. Other rats were stressed for 30 min and then returned to their home cage for 20 min before killing. Corticosterone and adrenocorticotropic hormone responses to restraint stress were significantly greater in EB-treated rats and lower in DHTP-treated rats at the 30-min timepoint compared to controls. c-fos mRNA increases following stress were augmented by EB but inhibited by DHTP. CRH hnRNA expression increased significantly in the PVN in response to restraint stress, and this increase was augmented by EB treatment, but decreased by DHTP treatment. Vasopressin hnRNA expression was also increased in response to stress, and this increase was attenuated by DHTP. These findings indicate that gonadal hormones influence the reactivity of the hypothalamic-pituitary adrenal axis to stress.
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PMID:Androgen inhibits, while oestrogen enhances, restraint-induced activation of neuropeptide neurones in the paraventricular nucleus of the hypothalamus. 1504 58


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