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.

Thyrotropin (TSH) Response to Synthetic TSH-Releasing Factor Following Pharmacological Blockade of Adrenocorticotropin (ACTH) Secretion

1972 ◽  
Vol 50 (4) ◽  
pp. 360-363 ◽  
Author(s):  
Bernard Koch ◽  
Michel Jobin ◽  
Serge Dulac ◽  
Claude Fortier
Keyword(s):  
Intravenous Injection ◽  
Plasma Corticosterone ◽  
Acth Secretion ◽  
Tsh Secretion ◽  
Corticosterone Response ◽  
Pharmacological Blockade ◽  
Nembutal Anesthesia

Pretreatment of rats with either dexamethasone or chlorpromazine, morphine, and Nembutal, though completely preventing the rise in plasma corticosterone and hence the release of ACTH otherwise associated with the intravenous injection of either saline or synthetic TSH-releasing factor (TRF) (200 ng), under ether or Nembutal anesthesia, failed to alter the plasma TSH response to TRF recorded 10 min after the injection. The plasma corticosterone response to the stress of the intravenous injection was of the same order in the animals injected with TRF as in the saline-injected controls. These findings fail to support the hypothesis of a competition between ACTH and TSH secretion at the pituitary level.

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 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.

scholarly journals Inflammatory Pain and Corticosterone Response in Infant Rats: Effect of 5-HT1A Agonist Buspirone Prior to Gestational Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Irina P. Butkevich ◽  
Viktor A. Mikhailenko ◽  
Tat'yana R. Bagaeva ◽  
Elena A. Vershinina ◽  
Anna Maria Aloisi ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Inflammatory Pain ◽  
Formalin Test ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Plasma Corticosterone Level ◽  
Infant Rats ◽  
Corticosterone Response ◽  
Gestational Stress

Our researches have shown that gestational stress causes exacerbation of inflammatory pain in the offspring; the maternal 5-HT1A agonist buspirone before the stress prevents the adverse effect. The serotonergic system and hypothalamo-pituitary-adrenal (HPA) axis are closely interrelated. However, interrelations between inflammatory pain and the HPA axis during the hyporeactive period of the latter have not been studied. The present research demonstrates that formalin-induced pain causes a gradual and prolonged increase in plasma corticosterone level in 7-day-old male rats; twenty-four hours after injection of formalin, the basal corticosterone level still exceeds the initial basal corticosterone value. Chronic treatments of rat dams with buspirone before restraint stress during gestation normalize in the offspring pain-like behavior and induce during the acute phase in the formalin test the stronger corticosterone increase as compared to the stress hormonal elevation in animals with other prenatal treatments. Negative correlation between plasma corticosterone level and the number of flexes+shakes is revealed in buspirone+stress rats. The new data enhance the idea about relativity of the HPA axis hyporeactive period and suggest that maternal buspirone prior to stress during gestation may enhance an adaptive mechanism of the inflammatory nociceptive system in the infant male offspring through activation of the HPA axis peripheral link.

Model for Korsakoff-Type Amnesias: Negative Effects from the Amygdala and Mamillary Body

1978 ◽  
Vol 43 (3) ◽  
pp. 767-770 ◽  
Author(s):  
B. P. H. Poschel ◽  
F. W. Ninteman
Keyword(s):  
Food Pellet ◽  
Learning Ability ◽  
Male Rats ◽  
Negative Effects ◽  
Mamillary Body ◽  
Hippocampal Stimulation ◽  
Set Up ◽  
Intracranial Electrodes ◽  
Stimulation Of ◽  
Daily Test

Intracranial electrodes were implanted bilaterally in the anterior area of the amygdala ( n = 7), or unilaterally in the mamillary body ( n = 6) of Hot: (SD) male rats. The rats were then trained to run back and forth to obtain food pellets at either end of a runway. At the midpoint were two adjacent doorways. Passing through the correct doorway set up food-pellet delivery. Passing through the incorrect doorway merely registered as an error. Daily test sessions lasted 25 min., and accumulated correct and incorrect runs were recorded for each session. The doorway designated as correct was changed each day throughout the training and testing period. On those days when the effects on learning of stimulation of the amygdalae or mamillary body were tested, the electrical brain stimulation was administered just prior to placing the rat in the runway. No detrimental effects on learning were associated with electrical stimulation of either brain structure. These findings are contrasted with our earlier study of hippocampal stimulation, which showed large deficits in learning ability.

Adrenocortical responses of ducks to treadmill exercise

1982 ◽  
Vol 94 (1) ◽  
pp. 141-146 ◽  
Author(s):  
S. Harvey ◽  
J. G. Phillips
Keyword(s):  
Treadmill Exercise ◽  
Plasma Corticosterone ◽  
Pretreatment Level ◽  
Corticosterone Concentration ◽  
Domestic Ducks ◽  
Corticosterone Secretion ◽  
Corticosterone Response ◽  
Response To Exercise ◽  
Adrenocortical Responses ◽  
Stationary Control

The influence of treadmill exercise on corticosterone secretion has been determined in domestic ducks. In birds unused to such exercise the concentrations of plasma corticosterone were markedly increased (> fourfold) after 15 or 30 min of treadmill exercise (1·1 km/h at 3 ° grade) and the level remained high (between 30 and 40 ng/ml) throughout 90 min of exercise. This increase in corticosterone secretion accompanied a similar increase in colon temperature and was independent of the plasma glucose level. After exercise the corticosterone concentration declined to the pretreatment level within 60 min of recovery. In birds used to the exercise the corticosterone response to a standard (30 min) period of exercise was diminished (by 77·6% in comparison with untrained birds and was no greater than the response (1·7-fold) in stationary control birds after handling and bleeding. The diminution of the corticosterone response to exercise may be due to the trained birds becoming fitter and better able to perform the work involved.

Effect of adenosine analogues on plasma corticosterone concentration in rats

1992 ◽  
Vol 127 (5) ◽  
pp. 471-475 ◽  
Author(s):  
Edmund Przegaliński ◽  
Bogusława Budziszewska ◽  
Anna Grochmal
Keyword(s):  
Adenosine Receptor ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Receptor Antagonists ◽  
Corticosterone Concentration ◽  
Adenosine Analogues ◽  
Negative Results ◽  
Corticosterone Secretion ◽  
Corticosterone Response ◽  
Pharmacological Blockade

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 × 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 30mg/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.

Effects of hypophysectomy and dexamethasone on rat adrenal response to microwaves

1979 ◽  
Vol 47 (6) ◽  
pp. 1284-1288 ◽  
Author(s):  
W. G. Lotz ◽  
S. M. Michaelson
Keyword(s):  
Plasma Corticosterone ◽  
Acth Secretion ◽  
Microwave Exposure ◽  
Hypophysectomized Rats ◽  
Integrative Process ◽  
Corticosterone Response ◽  
Adrenal Response ◽  
Prior Administration ◽  
Stimulation Of ◽  
Intact Rats

Circulating corticosterone levels were measured to compare the adrenocortical response to acute microwave exposure of normal, hypophysectomized, or sham-hypophysectomized rats. Plasma corticosterone levels in acutely hypophysectomized rats exposed to 60 mW/cm2 for 60 min were below control levels, indicating that the microwave-induced corticosterone response observed in normal, intact rats is dependent on ACTH secretion by the pituitary. In other groups of rats pretreated with dexamethasone before being exposed to microwaves for 60 min, the corticosterone response to a 50-mW/cm2 exposure was completely suppressed by doses equal to or greater than 3.2 micrograms dexamethasone/100 g body weight. However, the corticosterone response to a 70-mW/cm2 exposure was only partially suppressed by prior administration of 3.2 or 5.6 micrograms dexamethasone/100 g BW. The evidence obtained in these experiments, in conjunction with the results of other experiments previously reported, is consistent with the hypothesis that the stimulation of the adrenal axis in the microwave-exposed rat is a systemic, integrative process due to a general hyperthermia.

EFFECTS OF NORETHANDROLONE ON CORTISONE-INDUCED PITUITARY-ADRENAL SUPPRESSION IN THE RAT

1966 ◽  
Vol 52 (1) ◽  
pp. 25-29 ◽  
Author(s):  
Julian I. Kitay ◽  
M. D. Coyne
Keyword(s):  
Combined Therapy ◽  
Test Dose ◽  
Hepatic Metabolism ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Concomitant Treatment ◽  
Response To Stress ◽  
Corticosterone Response ◽  
Adrenal Corticosterone

ABSTRACT Norethandrolone administered to castrated male rats stimulated adrenal corticosterone production evaluated in vitro and increased pituitary content of corticotrophin (ACTH). Hepatic metabolism of corticosterone in vitro was unchanged. Concomitant treatment with norethandrolone and cortisone resulted in significantly greater adrenal corticosterone production in vitro compared to that obtained after cortisone treatment alone. Combined therapy also enhanced the plasma corticosterone response to a test dose of ACTH. No improvement was noted in the response to stress, offering no substantiation to the hypothesis that norethandrolone is of value in overcoming cortisone-induced depression of pituitary ACTH release.

scholarly journals The transformation of hormonal stress responses throughout puberty and adolescence

2011 ◽  
Vol 210 (3) ◽  
pp. 391-398 ◽  
Author(s):  
Allison R Foilb ◽  
Patina Lui ◽  
Russell D Romeo
Keyword(s):  
Stress Response ◽  
Adolescent Development ◽  
Stress Responses ◽  
Stress Reactivity ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Before And After ◽  
Corticosterone Response ◽  
Acute Stressor ◽  
Adrenal Corticosterone

Prepubertal rats display heightened hormonal stress reactivity compared with adults in that levels of ACTH and corticosterone take twice as long (i.e. 40–60 min) to return to baseline following an acute stressor. Despite this substantial change in stress responsiveness, and the critical nature of the adolescence period of development, the maturation of the hormonal stress response from the time of pubertal onset to adulthood has not been thoroughly investigated. To examine this, we measured ACTH, corticosterone, and testosterone in 30-, 40-, 50-, 60-, and 70-day-old (i.e. spanning pubertal and adolescent development) male rats before and after a 30 min session of restraint stress. We found that the adult-like ACTH stress response develops between 50 and 60 days of age, while the corticosterone response changes between 30 and 40 days of age. We also found that adrenal corticosterone concentrations paralleled the plasma corticosterone response following restraint, suggesting that stress-induced adrenal corticosterone synthesis decreases during adolescent development and may, at least in part, contribute to the differential stress response observed before and after puberty. Finally, stress leads to increases in testosterone secretion, but only after 50 days of age. Collectively, these results indicate that shifts in hormonal stress responses occur throughout adolescent maturation and that these responses show distinct developmental profiles.

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