Corticosterone Concentrations In Rats Research Articles

Study of heart rate and corticosterone variability in the simulation of rhino-surgical interventions in biological objects.

Aims: to assess changes in the time range of heart rate variability (HRV) and plasma corticosterone concentration in rats after simulating septoplasty. Materials and methods: a septoplasty was simulated in 30 mature male Wistar rats weighing 210-290 g. An ECG was recorded with subsequent analysis of the time domain of HRV, as well as blood sampling for changes in the concentration of corticosterone in the blood plasma. Results: SDNN significantly increased in comparison with the control on days 2 and 3 (p <0.001), but decreased on days 4-5 (p <0.001) and 6 days (p <0.01 ). rMSSD changed in waves with two irregular peaks on days 1 and 6. SDNN / rMSSD, in comparison with the 1st day of the postoperative period, increased on the 2nd day and continued to grow (p <0.05), and on the 4th day it began to decrease (p <0.01). The total power of HRV was low throughout the postoperative period (p <0.001), except for the 3rd day, when it was equal to the control data. The increase in the total power indicator fell on the 3rd day after the operation (p <0.01), after which its decline occurred again. The concentration of corticosterone in the blood plasma in rats was significantly higher than before (p <0.001). From the 2nd to the 4th postoperative day, its plateau was determined. Conclusion: Simulation of septoplasty leads to changes in the time range of HRV, an increase in the concentration of corticosterone in the blood plasma in rats with its maximum at the time of surgery and after 24 hours, the formation of a "plateau" from the 2nd to the 4th postoperative days, which coincides with changes of HRV.

Study of heart rate and corticosterone variability in the simulation of experimental rhino-surgical interventions.

Aims: to assess changes in the time range of heart rate variability (HRV) and plasma corticosterone concentration in rats after simulating septoplasty. Materials and methods: a septoplasty was simulated in 30 mature male Wistar rats weighing 210-290 g. An ECG was recorded with subsequent analysis of the time domain of HRV, as well as blood sampling for changes in the concentration of corticosterone in the blood plasma. Results: SDNN significantly increased in comparison with the control on days 2 and 3 (p <0.001), but decreased on days 4-5 (p <0.001) and 6 days (p <0.01 ). rMSSD changed in waves with two irregular peaks on days 1 and 6. SDNN / rMSSD, in comparison with the 1st day of the postoperative period, increased on the 2nd day and continued to grow (p <0.05), and on the 4th day it began to decrease (p <0.01). The total power of HRV was low throughout the postoperative period (p <0.001), except for the 3rd day, when it was equal to the control data. The increase in the total power indicator fell on the 3rd day after the operation (p <0.01), after which its decline occurred again. The concentration of corticosterone in the blood plasma in rats was significantly higher than before (p <0.001). From the 2nd to the 4th postoperative day, its plateau was determined. Conclusion: Simulation of septoplasty leads to changes in the time range of HRV, an increase in the concentration of corticosterone in the blood plasma in rats with its maximum at the time of surgery and after 24 hours, the formation of a "plateau" from the 2nd to the 4th postoperative days, which coincides with changes of HRV.

Sex-dependent and -independent regulation of thyrotropin-releasing hormone expression in the hypothalamic dorsomedial nucleus by negative energy balance, exercise, and chronic stress

The dorsomedial nucleus of the hypothalamus (DMH) is part of the brain circuits that modulate organism responses to the circadian cycle, energy balance, and psychological stress. A large group of thyrotropin-releasing hormone (Trh) neurons is localized in the DMH; they comprise about one third of the DMH neurons that project to the lateral hypothalamus area (LH). We tested their response to various paradigms. In male Wistar rats, food restriction during adulthood, or chronic variable stress (CVS) during adolescence down-regulated adult DMH Trh mRNA levels compared to those in sedentary animals fed ad libitum; two weeks of voluntary wheel running during adulthood enhanced DMH Trh mRNA levels compared to pair-fed rats. Except for their magnitude, female responses to exercise were like those in male rats; in contrast, in female rats CVS did not change DMH Trh mRNA levels. A very strong negative correlation between DMH Trh mRNA levels and serum corticosterone concentration in rats of either sex was lost in CVS rats. CVS canceled the response to food restriction, but not that to exercise in either sex. TRH receptor 1 (Trhr) cells were numerous along the rostro-caudal extent of the medial LH. In either sex, fasting during adulthood reduced DMH Trh mRNA levels, and increased LH Trhr mRNA levels, suggesting fasting may inhibit the activity of TRHDMH->LH neurons. Thus, in Wistar rats DMH Trh mRNA levels are regulated by negative energy balance, exercise and chronic variable stress through sex-dependent and -independent pathways.

Autogenous transplants of adrenal fragments in an animal model.

Autograft transplantation was performed on 3 groups of Sprague Dawley rats. In the first group, physiological corticosterone concentrations were determined. These animals were not operated. In the second group, both adrenal glands were removed. Corticosterone concentrations were determined after bilateral adrenalectomy. The third group was divided into two parts. In the first subgroup, bilateral adrenalectomy was performed simultaneosly with adrenal transplant into the omentum. In the second subgroup, right adrenalectomy was performed simultaneosly with and adrenal transplant into the omentum followed a month later by left adrenalectomy. During the experiment, corticosterone concentrations were measured at 4 time points. The statistical difference between corticosterone concentrations in rats after two timed adrenalectomies and rats after bilateral adrenalectomy was statistically different, but these results were far from physiological concentrations.

Соотношение между уровнем поведенческой активности, концентрацией циркулирующего кортикостерона у крыс с различной устойчивостью к гипоксии

Соотношение между уровнем поведенческой активности, концентрацией циркулирующего кортикостерона у крыс с различной устойчивостью к гипоксии

Effect of co-treatment with fluoxetine or mirtazapine and risperidone on the active behaviors and plasma corticosterone concentration in rats subjected to the forced swim test

BackgroundSeveral clinical reports have postulated a beneficial effect of the addition of a low dose of risperidone to the ongoing treatment with antidepressants in treatment-resistant depression. MethodsThe present study aimed to examine the effect of treatment with fluoxetine or mirtazapine, given separately or jointly with risperidone, on active behavior and plasma corticosterone level in male Wistar rats subjected to the forced swim test (FST). ResultsThe obtained results showed that fluoxetine (5mg/kg), mirtazapine (5 and 10mg/kg) or risperidone (0.05 and 0.1mg/kg) did not change the active behavior of rats in the FST. However, co-treatment with fluoxetine (10mg/kg) and risperidone (0.1mg/kg) induced an antidepressant-like effect in that test because it significantly increased the swimming time and decreased the immobility time, while combined treatment with mirtazapine at 5 and 10mg/kg and risperidone at 0.05 and 0.1mg/kg evoked a significant increase in the swimming time and also climbing, and decreased the immobility time. WAY 100635 (a 5-HT1a receptor antagonist) at a dose of 0.1mg/kg inhibited the antidepressant-like effect induced by co-administration of fluoxetine or mirtazapine and risperidone. Active behavior in that test did not reflect an increase in general activity, since combined treatment with fluoxetine or mirtazapine and risperidone failed to enhance the exploratory activity of rats. Co-treatment with fluoxetine or mirtazapine and risperidone did not reduce the stress-induced increase in plasma corticosterone concentration in animals subjected to the FST. ConclusionThe obtained results indicate that risperidone applied in a low dose enhances the antidepressant-like activity of fluoxetine and mirtazapine in the FST (but does not normalize the stress-induced increase in corticosterone level in these rats), and that 5-HT1a receptors may play some role in these effects.

Diallyl Disulfide Reduced Dose-Dependently the Number of Lymphocyte Subsets and Monocytes in Rats

Diallyl disulfide (DADS) is a major sulfur compound of garlic, and exerts anti-inflammatory, immune-modulatory, and enhancing sympathetic activity effects. However, it still remains unclear how DADS affects the distribution of white blood cell subsets, which is essential to execute effective immune responses and partially regulated by adrenal glucocorticoids. Therefore, we examined the dose-dependent effects of DADS administration on the circulating number of white blood cells (WBCs) and lymphocyte subsets, and plasma corticosterone concentration in rats. Male 10-wk-old Sprague Dawley rats were divided into the DADS-free and DADS-orally administered (dose=10, 20, and 40 mg/kg BW) groups. Blood samples were collected from the tail vein at 0, 1, 2, 4, and 6 h after the administration. DADS administration decreased dose- and time-dependently the circulating number of total WBCs, total lymphocytes, and monocytes. Within the lymphocyte subsets, the circulating number of T-lymphocytes and B-lymphocytes was significantly reduced 4 h after DADS administration in a dose-dependent manner, although that of natural killer (NK) cells was not affected. On the other hand, although DADS administration did not significantly change the circulating number of neutrophils, the circulating number of eosinophils and basophils showed a decreasing tendency after DADS administration. In contrast, plasma corticosterone concentration was increased 2 h after DADS administration in a dose-dependent manner. These results suggest that DADS administration reduces the circulating number of monocytes and lymphocytes, including especially acquired immune cells, via the action of corticosterone, and the effects are induced in a dose-dependent manner.

The effects of delta 9-tetrahydrocannabinol, cannabidiol, and shock on plasma corticosterone concentrations in rats.

The effects of delta 9-tetrahydrocannabinol, cannabidiol, and shock on plasma corticosterone concentrations in rats.

Lowering Effects of Allyl Isothiocyanate on the Number of Lymphocyte and Its Subsets in Rats

The purpose of this study was to elucidate the effects of a main pungent component of wasabi, allyl isothiocyanate (AITC), on the number of lymphocytes, T-lymphocyte, B-lymphocyte and natural killer (NK) cells and plasma corticosterone concentrations in rats. AITC was given as either single dosage [20 mg/kg body weight per day; subcutaneous (s.c.) and oral] or as a daily dosage (10 mg and 20 mg/kg body weight per day; s.c.) for 4 days for the hourly and daily assessment of changes in the numbers of lymphocytes, respectively. A single s.c. injection or oral administration of AITC significantly reduced the number of lymphocytes at 4 hr to approximately 0.68 times, indicating that decreased effects of AITC on the number of lymphocytes are independent on the administration route. Administration of AITC for 4 days reduced dose-dependently the number of lymphocytes, and significantly reduced the number of T-lymphocyte and B-lymphocyte to 0.79 and 0.60 times, respectively. However, the number of NK cells did not change by AITC. Administration of AITC increased plasma corticosterone concentrations at 4 day of post s.c. injection to 5.4-6.0 times. These results suggest that AITC-mediated immunosuppresion is at least in part attributable to changes in the number and distribution of lymphocyte and its subsets.

The influence of different dietary fat sources on tissue corticosterone concentration in rats

1. Local variation in helminth burdens of bank voles (Clethrionomys glareolus) from ecologically similar sites: temporal stability and relationships with hormone concentrations and social behaviour C.J. Barnard, K. Kulis, J.M. Behnke, A. Bajer, J. Gromadzka-Ostrowska, M. Stachon, E. Sinski Journal of Helminthology CrossRef

Serotonin receptors involved in regulation of pituitary-adrenocortical function in rats

Drugs that enhance brain serotonin function (direct agonists, serotonin uptake inhibitors and serotonin releasers) increase serum corticosterone concentration in rats, and in many cases ACTH has been shown to be similarly increased. At least two distinct serotonin receptor subtypes can mediate this effect. One is the 5-HT 1 A receptor, and the other seems to be a 5-HT 2 A receptor. Possibly, the 5-HT 2 C receptor or other receptors can also mediate these effects. The increase in serum corticosterone seems to be one useful marker in characterizing drug effects on serotonergic function. Much needs to be learned about the physiological importance and roles of this serotonergic influence on pituitary-adrenocortical function. Some studies have suggested it may be important in the diurnal rhythmicity of glucocorticoid secretion and perhaps in some stress effects. Serotonergic activation can also increase plasma levels of ACTH and cortisol in humans. Although the effects in humans are less well characterized than in rats, they seem to be useful as a way of probing brain serotonergic function in disease or after drug treatment. As more drugs that act selectively on a single receptor subtype become available for use in humans, more precise information about particular receptor subtypes should be attainable.

Decreased postnatal testosterone and corticosterone concentrations in rats following acute intermittent prenatal hypoxia without alterations in adult male sex behavior

The prenatal and postnatal testosterone surges in the male rat are associated with neurobehavioral sexual differentiation of the brain. Both surges can be attenuated by maternal stress or other environmental factors that activate the maternal and/or fetal hypothalamic/pituitary/adrenal (HPA) axis during the last week of gestation. Since hypoxia is known to activate the HPA axis, we studied its effect during gestation on sexual differentiation in the male rat. We examined the influence of intermittent hypoxic exposure during gestation with respect to the postnatal testosterone surge and corticosterone levels, and subsequent development of adult reproductive and nonreproductive sexually dimorphic behaviors. Plasma testosterone and corticosterone concentrations of male neonates were measured after maternal exposure to acute, intermittent, prenatal hypoxia (9% O 2 6 h/day from Day 15 to 21 of gestation). Relative to normoxic controls, acute, intermittent, prenatal hypoxia significantly attenuated the postnatal testosterone surge. Postpartum plasma corticosterone levels in these animals were also suppressed. In adulthood, prenatally hypoxic animals exhibited normal masculine sex behavior. Lordosis behavior in response to estrogen and progesterone priming was not significantly different between treatment groups. Saccharin preference, a nonreproductive, sexually dimorphic behavior, was not significantly influenced by prenatal hypoxic exposure. These results demonstrate that in the male acute intermittent prenatal hypoxia attenuates the postnatal testosterone surge. However, this reduction failed to result in significant alterations in the expression of sex related behaviors in adulthood.

Corticosterone Enhances the Zinc and Interleukin-6-Mediated Induction of Metallothionein in Cultured Rat Hepatocytes

The regulation of metallothionein induction in cultured rat hepatocytes was investigated with Zn, hormones, cytokines and either the synthetic glucocorticoid, dexamethasone, or the endogenous rat glucocorticoid, corticosterone. A concentration-dependent increase was seen with Zn (two- to fivefold increase in 24 h, Zn 10-50 mumol/L). Dexamethasone at 1 mumol/L increased metallothionein synthesis by fourfold that of the controls. Maximal metallothionein concentrations of 17-fold the control value were seen with 50 mumol/L Zn and 1 mumol/L dexamethasone. Interleukin-6 (1 x 10(5) U/L) alone did not induce metallothionein but increased it 35-65% with Zn+dexamethasone. Like dexamethasone, corticosterone had a dose dependent effect on metallothionein and synergy with Zn and Zn+interleukin-6. Dexamethasone was approximately 100 times more potent than corticosterone at 10-100 mumol/L. Physiological concentrations of corticosterone (1 mumol/L) when added alone, with Zn (10 mumol/L), and with Zn+interleukin-6 resulted in inductions of 2.2, 5.0 and 7.4-fold above the control cultures. Glucagon (1 mumol/L) had no independent effect but increased metallothionein by 31% and 33% with Zn(10 mumol/L)+dexamethasone (1 mumol/L) and Zn-dexamethasone+interleukin-6, respectively. There was no accumulation of metallothionein with interleukin-1 beta, tumor necrosis factor alpha or interferon gamma (1 x 10(5) U/L) alone, but interleukin-1 beta and tumor necrosis factor alpha enhanced the response obtained with Zn+dexamethasone with and without interleukin-6. Insulin (100 U/L) alone, caused metallothionein accumulation and further enhanced the response seen with Zn+dexamethasone+interleukin-6+glucagon. No additional enhancement was seen with interleukin 1 beta+tumor necrosis factor alpha+interferon. The results demonstrate that concentrations of corticosterone in rats with experimental inflammation facilitate metallothionein induction with Zn and interleukin-6.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of adenosine analogues on plasma corticosterone concentration in rats.

In this study we examined the effect of the adenosine analogues: N6-cyclohexyladenosine, L-N6-phenylisopropyladenosine and 5'-N-ethylcarboxamidoadenosine on the plasma corticosterone concentration in rats. It was found that N6-cyclohexyladenosine (0.1-3.0 mg/kg), L-N6-phenylisopropyladenosine (0.1-1.0 mg/kg) and 5'-N-ethylcarboxamidoadenosine (0.01-1.0 mg/kg) dose-dependently increased the plasma corticosterone level. The effects of N6-cyclohexyladenosine (0.1 mg/kg) and L-N6-phenylisopropyladenosine (0.1 mg/kg) were completely blocked in animals pretreated with dexamethasone (3 x 1 mg/kg), as well as in animals with a pharmacological blockade of the release of hypothalamic corticotropin-releasing factor induced by chloropromazine (10 mg/kg), morphine (20 mg/kg) and nembutal (25 mg/kg), whereas the corticosterone response to 5'-N-ethylcarboxamidoadenosine (0.01 mg/kg) was blocked in dexamethasone-pretreated rats only. On the other hand, the adenosine receptor antagonists: 8-(p-sulfophenyl)-theophylline (30 mg/kg), 8-phenyltheophylline (10 and 30 mg/kg), 1,3-dipropyl-8-(2-amino-4-chloro)-phenylxanthine (1 and 3 mg/kg) and 1,3-dipropyl-7-methylxanthine (1 mg/kg) did not affect the corticosterone response to N6-cyclohexyladenosine, L-N6-phenylisopropyladenosine or 5'-N-ethylcarboxamidoadenosine. The obtained results indicate that N6-cyclohexyladenosine and L-N6-phenylisopropyladenosine stimulate the corticosterone secretion at the hypothalamic level, whereas 5'-N-ethylcarboxamidoadenosine is likely to act at the pituitary level. Although the effects produced by the adenosine analogues show that both A1 and A2 receptors are involved in the corticosterone response, negative results of the interaction studies with adenosine receptor antagonists indicate that further experiments are necessary to elucidate this problem.

Effect of adenosine analogs on plasma corticosterone concentration in rats

Adenylate cyclase in homogenates of guinea pig ventricles was inhibited by the stable adenosine analogs N6-phenylisopropyl-adenosine (PIA) and 5′-N-ethylcarboxamidoadenosine (NECA). Inhibition required GTP and was enhanced by sodium ion. The maximum inhibition observed was 35.1±1.1%, the EC50 (95% confidence limits,n) for PIA and NECA were 0.20μM (0.17–0.25μM, 6) and 0.66 μM (0.26–1.7 μM, 4) respectively. 8-Phenyltheophylline (10 and 100 μM) and isobutylmethylxanthine (100 μM) antagonized the inhibitory effects of the adenosine analogs. These results indicate that adenosine receptors of the inhibitory type (RI or A1) are present in guinea pig myocardium and may mediate some of the cardiac responses to adenosine.

Induction of Drug Metabolism can be a Homeostatic Response

The invasion of the body by toxic agents, in addition to the specific effects, causes a stereotype non-specific response -stress-, and an adaptive phenomenon like drug metabolism. Reserpine or hydrocortisone, causing a typical stress response, produce increased plasma concentrations of corticosterone in rats. -Here it is shown that corticosterone administration once, or for three days twice daily (200 mumoles/kg) increase body resistance to zoxazolamine, methyprylon, and tetraethylammonium bromide, reduce their plasma concentrations and augment zoxazolamine, hexobarbital, and aniline in vitro drug metabolism (9000 g liver supernatant). This constitutes a good evidence that drug metabolism can be induced in response to need.

Effects of chlordiazepoxide, flumazenil and DMCM on plasma catecholamine and corticosterone concentrations in rats

The effects of drugs representing three classes of benzodiazepine (BDZ) receptor-acting agents on circulating corticosterone (CS), noradrenaline (NA) and adrenaline (A) were examined in unstressed rats. Intragastric administration of a single-dose of the inverse agonist 3-carbomethoxy-4-ethyl-6,7-dimethoxy-β-carboline (DMCM; 10 mg/kg) evoked 15-,4- and 1.5-fold increases in plasma CS, A and NA, respectively, as compared to control values. The DMCM-induced CS, A and NA rises were completely blocked by combined treatment with the BDZ antagonist flumazenil (Ro 15-1788; 20 mg/kg). Flumazenil given alone did not affect plasma hormone levels. Administration (either intragastrically or intraperitoneally) of a single-dose of the BDZ agonist chlordiazepoxide (CDP; 20 mg/kg) produced a 10- to 15-fold increase in plasma CS but caused no change in plasma NA and A contents. Pretreatment with flumazenil blocked the CDP-elicited release of CS. The findings indicate that the CNS mechanisms controlling pituitary-adrenocortical and sympatho-adrenal outflow under basal conditions are functionally linked to central-type BDZ receptor system(s). Drugs with agonist or inverse-agonist actions at these receptor sites can be differentiated from each other by their distinct effects on plasma NA and A, but not CS, release.

Repeated treatment with antidepressant drugs and/or electroconvulsive shock (ECS) does not affect the quinpirole-induced elevation of the serum corticosterone concentration in rats

The selective dopamine D2 receptor agonist quinpirole (0.03-1 mg/kg intra peritoneally) increased dose-dependently the serum corticosterone level in rats. The effect of the maximum dose of quinpirole (0.3 mg/kg intraperitoneally) was antagonized in a dose- dependent manner by the selective D2 receptor antagonist sulpiride (3-30 mg/kg intra peritoneally), but not by the selective D(1) receptor antagonist SCH-23390 (3 mg/kg intra peritoneally). Imipramine and amitriptyline (10 mg/kg per os), administered acutely or repeatedly (twice daily for 14 days), did not affect the corticosterone response to quinpirole (0.1 mg/kg intraperitoneally). The response was modified neither in animals treated repeatedly with electroconvulsive shock (ECS) (seven shocks every 2 days), nor after their combined repeated treatment with imipramine and ECS. The above results indicate that repeated treatment with antidepressant drugs and/or ECS does not affect the sensitivity of dopamine D2 receptors involved in the corticosterone response to quinpirole.

Brain benzodiazepine receptor-mediated effects on plasma catecholamine and corticosterone concentrations in rats

The effects of the benzodiazepine (BDZ) receptor agonist chlordiazepoxide (CDP) and antagonist flumazenil (Ro 15-1788), given alone and in combination, on basal and novel environment stress (NES)-elevated plasma noradrenaline (NA), adrenaline (A) and corticosterone (CS) contents were investigated. When administered on their own, a medium dose of CDP (2.5 mg/kg) and a moderate dose of flumazenil (5 mg/kg) did not affect basal hormone levels. However, flumazenil potentiated the NES-induced CS elevation and suppressed the NA rise in response to NES. The 2.5 mg/kg dose of CDP attenuated the NES-elicited rise of CS and A, without changing the NES-enhanced NA concentrations. High doses of CDP (10 and 12.5 mg/kg), which elevated basal CS levels, prevented a further CS increase by NES and completely abolished the NA and A response to NES. The CDP effects on CS and NA were antagonized by pretreatment with flumazenil, in contrast to the CDP effect on A which was not blocked. The data indicate that brain (central-type) BDZ receptor systems are involved in regulating the neurosympathetic and adrenocortical, but not adrenomedullary, responses to mild stress.

Serotonin Receptor Subtypes Involved in the Elevation of Serum Corticosterone Concentration in Rats by Direct- and Indirect-Acting Serotonin Agonists

The serum corticosterone concentration in rats was increased by injection of quipazine, a relatively nonselective serotonin (5-hydroxytryptamine; 5-HT) agonist, or 8-hydroxy-2-(di-n- propylamino)tetralin (8-OH-DPAT), a serotonin agonist selective for the 5-HT1A subtype of receptor. The quipazine-induced increase in serum corticosterone was antagonized by 17 different serotonin antagonists; of these, MDL 11939, pirenperone, setoperone, mianserin, LY 281067, ketanserin, ritanserin and clozapine have relatively selective affinity for the 5-HT2 subtype of receptor. The 8-OH-DPAT-induced increase in serum corticosterone was not antagonized by metergoline, the most potent antagonist of the quipazine effect, but was antagonized by pindolol or penbutolol, 5-HT1A receptor antagonists. Pindolol did not block the effect of quipazine. The results support earlier evidence that serum corticosterone concentration in rats can be increased by activation of either 5-HT1A or 5-HT2 receptors. Indirect-acting serotonin agonists - fluoxetine, L-5-hydroxytryptophan and p-chloroamphetamine - also increased serum corticosterone concentrations. The increases elicited by those agents, which earlier had been reported not to be blocked by metergoline pretreatment, also were not blocked by pretreatment with pindolol or with the combination of metergoline and pindolol. Thus, an involvement of a specific serotonin receptor subtype in the actions of these indirect agonists has not been established.