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

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.

1992 ◽  
Vol 127 (5) ◽  
pp. 471-475 ◽  
Author(s):  
Edmund Przegaliński ◽  
Bogusława Budziszewska ◽  
Anna Grochmal

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.


1972 ◽  
Vol 50 (4) ◽  
pp. 364-367 ◽  
Author(s):  
André Dupont ◽  
Edouard Bastarache ◽  
Elemer Endröczi ◽  
Claude Fortier

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.


1979 ◽  
Vol 47 (6) ◽  
pp. 1284-1288 ◽  
Author(s):  
W. G. Lotz ◽  
S. M. Michaelson

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.


1989 ◽  
Vol 122 (2) ◽  
pp. 535-543 ◽  
Author(s):  
S. A. Nicholson

ABSTRACT Intraperitoneal injection of caffeine (12·5–100 mg/kg) into rats caused a significant, dose-related increase in plasma corticosterone 2 h later, when the greatest response was measured. The corticosterone response to laparotomy stress or i.v. injection of ACTH(1–24) was unaffected by prior injection of caffeine. The response to stress or caffeine was unaffected by adrenal enucleation 28 days previously. In vitro, 10 mmol caffeine/l stimulated basal release of corticosterone from adrenal quarters and potentiated the response to a sub-maximal stimulatory concentration of cyclic AMP (cAMP). The drug had no effect on release stimulated by a sub-maximal concentration of ACTH(1–24). Release of ACTH from pituitary fragments incubated in vitro was stimulated in a dose-related manner by caffeine (0·01–10 mmol/l), and the responses to hypothalamic extract and sub-maximal concentrations of corticotrophin-releasing factor (CRF-41) or arginine vasopressin (AVP), but not cAMP, were significantly enhanced by 10 mmol caffeine/l. Release of immunoreactive CRF-41 (but not AVP) was significantly increased by caffeine (0·01–10 mmol/l) added to hypothalami incubated in vitro. The response to injection of caffeine in vivo was completely prevented by pharmacological blockade of endogenous CRF release. Taken together, these results show that caffeine at high concentrations can stimulate directly the release of the hormones of the hypothalamo-pituitary-adrenocortical axis in vitro, but the fact that these concentrations are unlikely to be reached after administration in vivo suggests that the effect of caffeine may be mediated centrally. Journal of Endocrinology (1989) 122, 535–543


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Hirotaka Shoji ◽  
Tsuyoshi Miyakawa

AbstractThe elevated plus maze test is a widely used test for assessing anxiety-like behavior and screening novel therapeutic agents in rodents. Previous studies have shown that a variety of internal factors and procedural variables can influence elevated plus maze behavior. Although some studies have suggested a link between behavior and plasma corticosterone levels, the relationships between them remain unclear. In this study, we investigated the effects of experience with a battery of behavioral tests, the wall color of the closed arms, and illumination level on the behavior and plasma corticosterone responses in the elevated plus maze in male C57BL/6J mice. Mice were either subjected to a series of behavioral tests, including assessments of general health and neurological function, a light/dark transition test, and an open field test, or left undisturbed until the start of the elevated plus maze test. The mice with and without test battery experience were allowed to freely explore the elevated plus maze. The other two independent groups of naïve mice were tested in mazes with closed arms with different wall colors (clear, transparent blue, white, and black) or different illumination levels (5, 100, and 800 lx). Immediately after the test, blood was collected to measure plasma corticosterone concentrations. Mice with test battery experience showed a lower percentage of open arm time and entries and, somewhat paradoxically, had lower plasma corticosterone levels than the mice with no test battery experience. Mice tested in the maze with closed arms with clear walls exhibited higher open arm exploration than mice tested in the maze with closed arms with black walls, while there were no significant differences in plasma corticosterone levels between the different wall color conditions. Illumination levels had no significant effects on any measure. Our results indicate that experience with other behavioral tests and different physical features of the maze affect elevated plus maze behaviors. Increased open arm time and entries are conventionally interpreted as decreased anxiety-like behavior, while other possible interpretations are considered: open arm exploration may reflect heightened anxiety and panic-like reaction to a novel situation under certain conditions. With the possibility of different interpretations, the present findings highlight the need to carefully consider the test conditions in designing experiments and drawing conclusions from the behavioral outcomes in the elevated plus maze test in C57BL/6J mice.


1988 ◽  
Vol 255 (4) ◽  
pp. E525-E530 ◽  
Author(s):  
L. Witek-Janusek

The neonatal rat is very sensitive to the lethal effects of bacterial endotoxin. Because of the adaptive importance of pituitary-adrenal secretions to stress, this study examined the ontogeny of the plasma corticosterone and adrenocorticotropic hormone (ACTH) responses to endotoxin. The lethal sensitivity of young rats to endotoxin ranged from 0.5 to 30 mg/kg (ip) in the 1- to 21-day-old rat. After endotoxin treatment, the 1- and 2-day-old rat showed marked elevations of corticosterone similar in magnitude to that seen in 21-day-old and adult rats; however, significantly depressed corticosterone increments were observed in the 5-, 10-, and 14-day-old rats. This age-related pattern of adrenocortical secretion was correlated with the developing rat's corticosterone response to exogenous ACTH. In contrast, endotoxin administered to 5-, 10-, and 14-day-old rats resulted in increments of plasma ACTH similar to those observed in the 21-day-old and adult rats. Although plasma ACTH levels increased by 84-127% in the 1- and 2-day-old rats, these increases were significantly less than those of rats at all other ages tested. Thus the newborn rat mounts an effective corticosterone response to endotoxin, loses this ability between ages 5-14 days, and regains this response at 21 days of age. Because the hyporesponsive ages exhibit a marked increase in ACTH secretion, the loss of the adrenocortical response to endotoxin appears to be a result of a depressed responsiveness of the adrenal cortex to ACTH.


Neuroscience ◽  
2003 ◽  
Vol 116 (2) ◽  
pp. 553-563 ◽  
Author(s):  
C.H Summers ◽  
T.R Summers ◽  
M.C Moore ◽  
W.J Korzan ◽  
S.K Woodley ◽  
...  

1986 ◽  
Vol 250 (1) ◽  
pp. E87-E93
Author(s):  
W. C. Engeland

Comparisons of resting plasma adrenocorticotropin (ACTH) and corticosterone in the morning and afternoon were made among adult rats bearing regenerated adult adrenal grafts, neonatal (day 1) adrenal grafts, adult adrenal capsule grafts, or intact adrenals. In the morning plasma ACTH and corticosterone were similar in all rats. In the afternoon, plasma ACTH was elevated in rats bearing neonatal adrenal grafts or adult adrenal capsule grafts, but not in rats bearing whole adult adrenal grafts. There was no difference in afternoon plasma corticosterone among rats bearing transplanted adrenals, although afternoon plasma corticosterone was decreased in rats bearing transplants compared with rats with intact adrenals. Thus the increased plasma ACTH after adrenal transplantation cannot be explained entirely by decreases in resting plasma corticosterone. Adrenal responsiveness to ACTH was tested at 5 wk after transplantation in the afternoon by measuring the plasma corticosterone response to submaximal doses of ACTH. The responsiveness was decreased in rats bearing transplants. In addition, responsiveness was inversely related to the age of the grafted adrenal tissue. Adrenals regenerated from adult adrenals were more responsive than adrenals regenerated either from neonatal adrenals or from adult adrenal capsules. The findings suggest that following adrenal transplantation reestablishment of normal pituitary-adrenocortical function does not occur in rats bearing adrenals regenerated from immature adrenal cells. In addition, comparable alterations occur after regeneration of adrenal tissue from neonatal adrenal cells and adult adrenal capsular cells. Elevated plasma ACTH associated with adequate plasma corticosterone in rats bearing adrenals regenerated from immature adrenal cells may result from chronic alteration in responsiveness to steroid feedback.(ABSTRACT TRUNCATED AT 250 WORDS)


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