R. Collu

Shift in adenohypophyseal activity during chronic intermittent immobilization of rats

Female rats were subjected to 8 h of daily immobilization for 1, 3, 6, 10 or 15 days. Exposure for 3 days inhibited b.w. and induced adrenal enlargement as well as thymus involution; 6 days of stress

Pattern of adenohypophyseal hormone changes in male rats following chronic stress.

To delineate the pattern of adenohypophyseal hormone secretion following chronic stress, adult male rats were exposed daily to 6 h of cold, forced exercise or immobilization for 3, 6, 10, 15, 28 or 42 consecutive days. Groups of these animals were sacrificed at the end of the last stress sessions, and plasma growth hormone (GH), luteinizing hormone (LH), prolactin (Prl) and follicle-stimulating hormone (FSH) levels were measured by radioimmunoassay (RIA). Irresspective of the different stimuli used, long-term stress induced a morphologic and hormonal response characterized by decreased ponderal growth, adrenal enlargement, thymus involution and significant diminutions in GH, Prl and LH levels with no modifications in FSH titers. The magnitude and duration of these changes varied with the severity of the stressors.

Effects of thyrotropin-releasing hormone on behavioral and hormonal changes induced by β-endorphin

Abstract Adult male rats were injected intraventricularly either with saline or TRH (10 μg) 5 min prior to a second injection of either saline or β-endorphin (50 μg). The tripeptide produced a 100% increase of motility counts recorded over a 15 min period following the last injection, whereas β-endorphin decreased general motor activity. TRH pretreatment completely abolished the depressant effect of β-endorphin. In addition, TRH enhanced the PRL secretion induced by β-endorphin and antagonized the slight elevation of plasma GH levels observed in β-endorphin-treated rats. These results do not seem to be related to an interaction of TRH with opiate receptors since the tripeptide (10 −8 , 10 −6 M) added in vitro to rat brain homogenates did not alter the specific binding of 3 H-naloxone nor affect the displacement by β-endorphin of such binding.

The Montreal Type A Intervention Project: Major findings.

This article reports a comparison of three short-term treatments (aerobic exercise, cognitive-behavioral stress management, and weight training) in modifying behavioral and cardiovascular reactivity to laboratory psychosocial stressors in healthy Type A men. One hundred seven men completed the treatments and evaluations, 33 in the aerobic exercise group, and 37 each in the cognitive-behavioral stress management and weight-training groups. The stress management group showed significantly greater changes in behavioral reactivity (reductions of 13% to 23% below initial values) than the two physical exercise groups, which did not differ significantly from each other. For physiological reactivity, changes attributable to intervention were trivial for all three treatment groups. The positive finding of reduced behavioral reactivity as a result of the stress management intervention is of potential clinical significance and warrants further exploration. The lack of meaningful reductions in physiological reactivity also requires further exploration in that it raises questions concerning the ability of behavioral treatments in general to modify physiological reactivity, the ability of existing measures to assess accurately changes that are produced and, most fundamental of all, the relevance of physiological reactivity as an outcome measure for treatment efforts with Type As.

Hormonal modifications induced by chronic stress in rats

Abstract Chronic stress has a generally inhibitory effect on pituitary-gonadal function both in female and male rats inducing low circulating levels of LH, testosterone (T), prolactin (Prl) and, inconsistently, FSH. This inhibitory effect does not seem to be primarily due to pituitary dysfunction, since the adenohypophysis was capable of responding to exogenously administered LHRH and TRH, but is presumably the consequence of alterations of hypothalamic factor turnover. Testicular receptors to hCG were not modified by chronic stress which however induced a state of relative testicular hyper-responsiveness to hCG. Adrenal steroids seem to play a role both in the regulation of testicular hCG receptors and in chronic stress-induced Prl decrease, although further studies are needed to better characterize such a role.

Prevention by bombesin of cold-restraint stress induced hemorrhagic lesions in rats

Abstract Several neuropeptides, injected intraventricularly (ivt), were assessed for their effects on cold-restraint-induced hypothermia and hemorrhagic gastric lesions in 24 hr fasted rats. Bombesin (5-1 μg) further enhanced the drop in body temperature following stress and markedly prevented the gastric erosions in a dose-dependent fashion (5-0.1 μg). β-endorphin exerted a similar effect, but only at the 5 μg dose level. Other peptides (neurotensin, substance P, somatostatin and TRH: 5 μg) did not influence susceptibility to the gastric mucosal damage. Somatostatin and TRH reduced the hypothermic effect of stress. Bombesin is 250 times less potent when injected systemically than ivt and its actions are not reversed by nalaxone. The prevention of gastric erosions by bombesin could initially involve a central mechanism of action, independent of opiate receptors and possibly related to the sustained and marked hyperglycemia observed in bombesin treated rats exposed to stress.

Carbohydrate intolerance in children and adolescents with Turner syndrome

Carbohydrate homeostasis was evaluated in 41 girls, 6 to 20 years of age, with Turner syndrome by means of oral and intravenous glucose tolerance tests, as well as intravenous tolbutamide. Mean (±SE) glucose levels following oral glucose were higher at 60 minutes (162±5 vs 134±6 mg/dl, 2 P P P

Exaggerated psychophysiological reactivity: Issues in quantification and reliability

Marked physiological reactivity to challenging mental tasks has been associated with elevated risk for, as well as the presence of, coronary heart disease. However, little systematic enquiry into the reliability and quantification of such exaggerated reactivity has emerged. Subjects were 32 male, managerial employees, ranging in age from 22 to 56 yr, who satisfied the following criteria: no history or current signs of heart disease, presence of Type A behavior pattern as revealed by the Structured Interview, and an increase during an initial psychosocial stress testing of at least 25% over baseline in at least three out of five psychophysiological indices. Heart rate, systolic blood pressure, diastolic blood pressure, plasma epinephrine and plasma norepinephrine levels were monitored while challenging mental tasks were performed in three sessions (screening, pretraining and posttraining) spaced several weeks apart. Psychophysiological reactivity during the tasks emerged as a consistent trait. For all five measures, change scores from baseline during the screening session were significantly correlated with change scores during the pretraining session. Moreover, the magnitude of the change scores were similar in the screening and pretraining sessions. Analysis of cross correlations within and between indices provided little support for the use of data transformations such as residual scores or analysis of covariance. Finally, on four out of five measures, the challenging tasks were found to be comparable in the degree of reactivity elicited. These findings suggest that, for selected Type A men, exaggerated psychophysiological reactivity occurs reliably when monitored with multiple indices, appears insensitive to mere passage of time, and can be uniformly elicited by a variety of tasks.

G protein modulation by estrogens

Levels of various G protein subunits were assayed by immunoblot and densitometry, using specific antibodies, in anterior pituitaries and striata of female rats exposed to physiological or pharmacological modifications of ovarian hormone levels and, for comparison, in the same tissues of coeval male rats. Treatment of ovariectomized rats with 17 beta-estradiol 10 micrograms/rat/day for 5, 10 or 20 days induced a time-dependent rise in plasma prolactin (PRL) levels. While no change in G protein levels was observed in the striatum, estrogen treatment induced a significant reduction of all pituitary G protein levels except those of alpha i1, which remained unchanged, and of alpha s42, which increased in a time-dependent manner. A highly significant correlation was observed between pituitary alpha s42 values and plasma PRL levels. During the estrous cycle, pituitary values of alpha o, alpha i3 and alpha s47 were generally lower than those of ovariectomized rats, suggesting the existence of tonic inhibitory influence of circulating ovarian hormones. Pituitary levels of alpha o, alpha i1 and alpha s42 also showed a significant modulation during the various phases of the estrous cycle, and those of alpha o, alpha i3, alpha s47 and beta were significantly lower in female than in male rats. No significant effects of estrous cycle hormone variations or sex differences were observed in the values of striatum G proteins. In conclusion, these data clearly indicate that ovarian hormones, and particularly estrogens, have a significant and specific effect on pituitary G protein levels which may modulate the secretion of pituitary hormones such as PRL.

Effect of Stress and Hypothalamic Deafferentation on the Secretion of Growth Hormone in the Rat

Stressful stimuli are known to inhibitthe secretion of radioimmunoassayable rat growth hormone (RGH). Groups of adult male rats submitted to one of three different types of hypothalamic deafferentation (total, incomplete, or frontal) were exposed to ether and auditory stresses at 1 week intervals. Ether and auditory stresses were equally effective in inhibiting the RGH secretion in controls and frontally deafferented rats. Ether stress inhibited the RGH values of completely deafferented animals, while auditory stress left these values unchanged; α-MT pretreatment blocked the effect of ether stress in such animals. Neither stress was able to modify the already low values of the incompletely deafferented rats; pentobarbital anesthesia induced a marked rise of RGH plasma levels in these animals. Base-line levels of RGH were significantly higher in frontally deafferented, and significantly lower in incompletely deafferented rats than those of controls. These data seem to indicate that ether stress is transmitted through a humoral, dopa-minergic pathway, while auditory stress follows a nervous pathway. In addition, extra-hypothalamic influences seem to modulate the secretion of RGH through frontal inhibitory and postero-lateral stimulatory nervous pathways.