scholarly journals Corticosterone Levels in the Brain Show a Distinct Ultradian Rhythm but a Delayed Response to Forced Swim Stress

Endocrinology ◽  
2008 ◽  
Vol 149 (7) ◽  
pp. 3244-3253 ◽  
Author(s):  
Susanne K. Droste ◽  
Lotte de Groote ◽  
Helen C. Atkinson ◽  
Stafford L. Lightman ◽  
Johannes M. H. M. Reul ◽  
...  
Keyword(s):  
Pulse Frequency ◽  
Plasma Corticosterone ◽  
Stress Conditions ◽  
Male Rats ◽  
Ultradian Rhythm ◽  
Delayed Response ◽  
Corticosterone Concentration ◽  
Rapid Sampling ◽  
The Brain

Circulating corticosterone levels show an ultradian rhythm resulting from the pulsatile release of glucocorticoid hormone by the adrenal cortex. Because the pattern of hormone availability to corticosteroid receptors is of functional significance, it is important to determine whether there is also a pulsatile pattern of corticosterone concentration within target tissues such as the brain. Furthermore, it is unclear whether measurements of plasma corticosterone levels accurately reflect corticosterone levels in the brain. Given that the hippocampus is a principal site of glucocorticoid action, we investigated in male rats hippocampal extracellular corticosterone concentrations under baseline and stress conditions using rapid-sampling in vivo microdialysis. We found that hippocampal extracellular corticosterone concentrations show a distinct circadian and ultradian rhythm. The PULSAR algorithm revealed that the pulse frequency of hippocampal corticosterone is 1.03 ± 0.07 pulses/h between 0900 and 1500 h and is significantly higher between 1500 and 2100 h (1.31 ± 0.05). The hippocampal corticosterone response to stress is stressor dependent but resumes a normal ultradian pattern rapidly after the termination of the stress response. Similar observations were made in the caudate putamen. Importantly, simultaneous measurements of plasma and hippocampal glucocorticoid levels showed that under stress conditions corticosterone in the brain peaks 20 min later than in plasma but clears concurrently, resulting in a smaller exposure of the brain to stress-induced hormone than would be predicted by plasma hormone concentrations. These data are the first to demonstrate that the ultradian rhythm of corticosterone is maintained over the blood-brain barrier and that tissue responses cannot be reliably predicted from the measurement of plasma corticosterone levels.

Adrenocortical function in aging exercise-trained rats

1977 ◽  
Vol 43 (5) ◽  
pp. 839-843 ◽  
Author(s):  
J. A. Severson ◽  
R. D. Fell ◽  
J. G. Tuig ◽  
D. R. Griffith
Keyword(s):  
Age Groups ◽  
Plasma Corticosterone ◽  
Treadmill Running ◽  
Adrenocortical Function ◽  
Elevated Plasma ◽  
Corticosterone Concentration ◽  
Relationship Of ◽  
The Relationship

Plasma corticosterone concentrations and in vitro adrenal secretion of corticosterone were determined in exercise-trained rats. Rats, 100, 200, and 300 days of age, were trained for a 10-wk period by treadmill running. Following the training program, rats were subjected to an acute bout of swimming. Acute swimming elevated plasma corticosterone concentrations in all age groups. At 170 days of age, the plasma corticosterone concentration following swimming was higher in exercise-trained rats than in controls. The opposite was true of acutely swum rats at 270 and 370 days of age. Acute swimming elevated the in vitro adrenal gland response to adrenocorticotropic hormone stimulation in control rats at all ages and in trained rats at 170 days of age. The in vivo relationship of epinephrine and the pituitary adrenal system is suggested as a mechanism which could have caused this response. The relationship of secretion rates to plasma corticosterone concentrations indicated that extra-adrenal mechanisms, such as decreased turnover, were also responsible for the elevated plasma corticosterone levels observed in response to acute swimming.

Interleukin 1 stimulation of the hypothalamic-pituitary-adrenal axis

1990 ◽  
Vol 258 (1) ◽  
pp. E65-E70 ◽  
Author(s):  
A. R. Gwosdow ◽  
M. S. Kumar ◽  
H. H. Bode
Keyword(s):  
Interleukin 1 ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Plasma Acth ◽  
Organ Cultures ◽  
Intact Male ◽  
Corticosterone Concentration ◽  
Protein Binding Assay ◽  
Hypophysectomized Rats ◽  
Induced Changes

The effect of varying doses of purified human interleukin 1 (IL-1) on rectal temperature (Tr), hypothalamic corticotropin-releasing hormone (CRH), pituitary and plasma adrenocorticotropic hormone (ACTH), and plamsa corticosterone was examined in intact male rats at 24 degrees C; plasma ACTH and corticosterone responses were also studied in hypophysectomized rats. In addition, IL-1-induced changes in corticosterone concentration were investigated by means of adrenal organ cultures. Tr was measured with thermocouples. CRH and ACTH levels were determined by radioimmunoassay, and corticosterone by protein-binding assay. Intravenous administration of IL-1 (0.063-1.0 ng) resulted in hyperthermia, which began 20 min postinjection and continued for an additional 30 min. IL-1 at a dose of 0.5 ng resulted in no change in hypothalamic CRH, pituitary ACTH, or plasma ACTH levels compared with saline-treated rats. Plasma corticosterone was significantly (P less than 0.05) elevated 30 min after IL-1 administration and returned to control levels after 1 h. The higher dose of IL-1 (1.0 ng) did not affect hypothalamic CRH content, but pituitary ACTH began to rise at 15 min and was significantly (P less than 0.05) elevated 30 min after injection. Rats receiving this dose displayed elevated (P less than 0.05) plasma ACTH and corticosterone levels 30 and 60 min postinjection. No change in plasma corticosterone was observed in hypophysectomized rats administered either 1 ng of IL-1 or 1 microgram of recombinant IL-1 beta (rIL-1 beta); adrenal organ cultures treated with IL-1 (10(-11) M) responded similarly.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals A Possible Mechanism for the Action of Adrenomedullin in Brain to Stimulate Stress Hormone Secretion

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 4890-4896 ◽  
Author(s):  
Meghan M. Taylor ◽  
Willis K. Samson
Keyword(s):  
Hpa Axis ◽  
Hormone Secretion ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Stress Hormone ◽  
Elevated Plasma ◽  
The Central Nervous System ◽  
Neuroendocrine Responses ◽  
The Brain

Abstract Adrenomedullin (AM) has been reported to have actions at each level of the hypothalamo-pituitary-adrenal (HPA) axis, suggesting that the peptide plays a role in the organization of the neuroendocrine responses to stress. We examined the mechanism by which AM regulates the central nervous system branch of the HPA axis as well as the possible role of AM in the modulation of the releases of two other hormones, prolactin and GH, whose secretions also are altered by stress. Intracerebroventricular administration of AM led to elevated plasma corticosterone levels in unrestrained, conscious male rats. This effect was abrogated by pretreatment with a CRH antagonist, suggesting that AM activates the HPA axis by causing the release of CRH into hypophyseal portal vessels. In addition, AM given intracerebroventricularly stimulated the release of prolactin but did not alter the secretion of GH. We propose that AM produced in the brain may be an important neuromodulator of the hormonal stress response.

scholarly journals Protective effect of Curcumin against rotenone-induced Substantia nigra pars compacta neuronal dysfunction

2021 ◽  
Author(s):  
Lilit Vahan Darbinyan ◽  
Lilia Eduard Hambardzumyan ◽  
Larisa Paylak Manukyan ◽  
Karen Vazgen Simonyan ◽  
Carlos Augusto Carvalho de Vasconcelos ◽  
...  
Keyword(s):  
Substantia Nigra ◽  
Dopaminergic Neurons ◽  
Therapeutic Agent ◽  
Male Rats ◽  
Substantia Nigra Pars Compacta ◽  
Nissl Staining ◽  
Histological Changes ◽  
Naturally Occurring ◽  
The Brain

Abstract Rotenone is involved in the degeneration of dopaminergic neurons, and curcumin may prevent or effectively slow the progression of Parkinson disease (PD). Previous research has shown that the naturally occurring phenolic compound curcumin can reduce inflammation and oxidation, making it a potential therapeutic agent for neurodegenerative diseases. The present study involves investigation of rotenone induced histological changes in the brain areas, hippocampus using Nissl staining after 35 day of subcutaneous injection administration of rotenone in adult male rats. In this study, we investigated whether curcumin protects against rotenone-induced dopaminergic neurotoxicity in a rat model by in vivo electrical recording from Substantia nigra pars compacta (SNc). Curcumin treatment significantly improved electrical activity of neurons in the SNc of rotenone-induced PD model rats. The pattern of histological alterations corresponds with electrophysiological manifestations.

Differential role of glucocorticoids in mediating endotoxin-induced changes in IGF-I and IGFBP-1

1997 ◽  
Vol 272 (6) ◽  
pp. R1990-R1997 ◽  
Author(s):  
Y. H. Li ◽  
J. Fan ◽  
C. H. Lang
Keyword(s):  
Plasma Corticosterone ◽  
Mrna Abundance ◽  
Male Rats ◽  
Ru 486 ◽  
Igf I ◽  
Igf Binding ◽  
Induced Changes ◽  
Igf Binding Protein

The purpose of the present study was to determine whether endogenous elevations in glucocorticoids mediate the changes in insulin-like growth factor (IGF) 1 and IGF binding protein (IGFBP) 1 levels in plasma and tissues observed after in vivo administration of lipopolysaccharide (LPS). In overnight-fasted male rats LPS injected via the tail vein decreased the IGF-I concentration in plasma, liver, and skeletal muscle (30-45%) and increased IGF-I content in kidney (approximately 3-fold). LPS also decreased IGF-I mRNA abundance in liver and muscle and increased gene expression in kidney. Concomitantly, IGFBP-1 levels in plasma, liver, and muscle were markedly elevated by LPS. All these changes were associated with a greater than fourfold elevation in plasma corticosterone. Pretreatment of rats with the glucocorticoid receptor antagonist RU-486 completely prevented or blunted the LPS-induced changes in IGF-I content in plasma, liver, muscle, and kidney. In liver and muscle RU-486 significantly attenuated the reduction in IGF-I mRNA abundance produced by LPS, but in kidney the LPS-induced increase in IGF-I mRNA was still evident. In contrast, pretreatment with RU-486 did not prevent or attenuate the LPS-induced increase in IGFBP-1 levels in plasma, liver, or muscle. These data suggest that glucocorticoids play a major role in regulating IGF-I mRNA and peptide content in tissues in response to LPS, but the increased IGFBP-1 in blood and tissues induced by LPS appears largely glucocorticoid independent.

Catecholamine turnover in the brain and the regulation of luteinizing hormone and corticosterone in starved male rats

1982 ◽  
Vol 100 (2) ◽  
pp. 168-176 ◽  
Author(s):  
K. M. Pirke ◽  
B. Spyra
Keyword(s):  
Luteinizing Hormone ◽  
Wistar Rats ◽  
Preoptic Area ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Dopamine Turnover ◽  
Noradrenergic Neurons ◽  
Catecholamine Turnover ◽  
Male Wistar Rats ◽  
The Brain

Abstract. The effect of starvation was studied in male Wistar rats. After only 2 days of food deprivation, LH concentrations in serum are greatly suppressed, while a significant increase in plasma corticosterone occurs after 5 days' starvation. The noradrenaline and dopamine turnover in the basal hypothalamus is decreased after 2 days. The catecholamine turnover is also reduced in the preoptic area, and in the median eminence. Injection of the catecholamine precursor l-dopa (100 mg/kg) can prevent the increase of plasma corticosterone, but not the decrease of LH. The α-agonist clonidine (150 μg/kg), but neither the β-agonist salbutamol (0.5 mg/kg), nor the dopamine agonist apomorphine (1.0 mg/kg) can prevent the starvation induced corticosterone increase. The decrease of plasma LH is not influenced by the dopamine or noradrenaline agonists. From these data, it appears that a decreased activity of noradrenergic neurons may be responsible for the corticosterone increase in the plasma of starved rats.

EFFECTS OF TESTOSTERONE ON PITUITARY CORTICOTROPHIN AND ADRENAL STEROID SECRETION IN MALE AND FEMALE RATS

1963 ◽  
Vol 43 (4) ◽  
pp. 601-608 ◽  
Author(s):  
Julian I. Kitay
Keyword(s):  
Plasma Corticosterone ◽  
Female Rats ◽  
Male Rats ◽  
Intact Male ◽  
Male And Female ◽  
Adrenal Steroid ◽  
Adrenal Steroidogenesis ◽  
Male And Female Rats

ABSTRACT Administration of a depot testosterone preparation to male and female rats resulted in no change in body or pituitary weight in either sex. Pituitary corticotrophin content was unaltered in male animals but was reduced in females. Adrenal weights and adrenal RNA and DNA contents were decreased in both sexes. Plasma corticosterone concentrations were unaffected in males but were reduced in female rats after stress or corticotrophin injection. Hepatic reduction of ring A in vitro and biological half-life of corticosterone in vivo were unchanged in male animals but impaired in females. Testosterone administration to intact male rats significantly increased adrenal steroidogenesis measured in vitro. A significant decrease in steroid production was found in intact females but increased steroidogenesis was observed in adrenals from testosterone-treated oophorectomized animals. No effect was obtained following addition of testosterone directly in vitro. The data suggest that testosterone leads both to diminution of corticotrophin secretion and enhancement of adrenal steroid secretory capacity. In intact female rats, these effects are complicated by suppression of oestrogen secretion, the effects of which have been reported previously.

scholarly journals Short-term effects of corticosterone treatment on muscle protein synthesis in relation to the response to feeding

1987 ◽  
Vol 248 (2) ◽  
pp. 439-442 ◽  
Author(s):  
P J Garlick ◽  
I Grant ◽  
R T Glennie
Keyword(s):  
Protein Synthesis ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Liver Protein ◽  
Carrier Medium ◽  
Corticosterone Treatment ◽  
Small Inhibition

1. Rates of protein synthesis in liver and muscle of 100 g male rats were measured in vivo at 1 h or 4 h after injection of 2.5 mg of corticosterone and compared with those from animals given carrier medium alone. 2. In post-absorptive rats, corticosterone for 1 h had no effect on either muscle or liver protein synthesis. After 4 h there was a decrease in both tissues, but this was only statistically significant in muscle. 3. In fed rats, rates of protein synthesis were higher than those in post-absorptive animals, but the effects of corticosterone injection were similar. 4. Re-feeding of post-absorptive rats led to an increase in muscle protein synthesis after 1 h and 4 h. At 1 h this increase was not inhibited when plasma corticosterone concentrations were maintained high by injection of the hormone immediately before feeding commenced, but at 4 h there was a small inhibition. 5. It is concluded that the action of corticosterone in depressing muscle protein synthesis is time-dependent and requires longer than 1 h to develop. The failure of the hormone to alter the response to re-feeding for 1 h in post-absorptive rats suggest that corticosteroids are not important mediators of the acute stimulation of muscle protein synthesis by food intake.

Effect of Hippocampal Stimulation on the Plasma Thyrotropin (THS) and Corticosterone Responses to Acute Cold Exposure in the Rat

1972 ◽  
Vol 50 (4) ◽  
pp. 364-367 ◽  
Author(s):  
André Dupont ◽  
Edouard Bastarache ◽  
Elemer Endröczi ◽  
Claude Fortier
Keyword(s):  
Plasma Corticosterone ◽  
Male Rats ◽  
Bipolar Electrode ◽  
Corticosterone Concentration ◽  
Hippocampal Stimulation ◽  
Hippocampal Activity ◽  
Tsh Secretion ◽  
Corticosterone Response ◽  
A Minor ◽  
Stimulation Of

Seven days after the stereotaxic implantation of a bipolar electrode in the gyrus dentatus of the hippocampus of adult male rats, exposure to cold (20 min at −5 °C) increased both plasma TSH and corticosterone concentrations, whereas exposure in association with a minor environmental disturbance (presence of an observer) suppressed the TSH response to cold and enhanced the corticosterone response. Concurrent stimulation of the hippocampus with monophasic square waves of 1.3–1.5 V, 10 c.p.s., and 0.1 ms duration was found to restore the TSH response to cold and to inhibit the secretion of adrenocorticotropin (ACTH) (as reflected by the plasma corticosterone concentration). These findings suggest that the concurrent stimulation of ACTH release and inhibition of TSH secretion induced by nonspecific stress are possibly related to depressed hippocampal activity.

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