DHEA administration increases rapid eye movement sleep and EEG power in the sigma frequency range.

Dehydroepi-androsterone (DHEA) exhibits various behavioral effects in mammals, at least one of which is enhancement of memory that appears to be mediated by an interaction with the gamma-aminobutyric acidA (GABAA) receptor complex. We investigated the effects of a single oral dose of DHEA (500 mg) on sleep stages, sleep stage-specific electroencephalogram (EEG) power spectra, and concurrent hormone secretion in 10 healthy young men. DHEA administration induced a significant (P < 0.

The hypothalamic-pituitary-adrenocortical system and sleep in man.

This review article summarizes the major findings about the interactions of human sleep structure and the hypothalamo-pituitary-adrenocortical (HPA) system under physiological and pathophysiological conditions, including studies that probe the sleep effects of systemically administered HPA hormones. Human sleep is regulated by a concerted action of various signal compounds acting at sleep-generating neurons whose central organization is not yet fully understood. During nocturnal sleep the endocrine system is remarkably active, the longest established finding being that growth hormone (GH) release is associated with the initiation of sleep and that there is a steep morning rise of cortisol (Weitzman et al.

Effects of 5HT3 receptor antagonism by tropisetron on the sleep EEG and on nocturnal hormone secretion.

Two dosages (5 mg and 25 mg) of the selective 5HT3 receptor antagonist tropisetron (ICS 205-930) were administered to healthy male controls, and the effects on the sleep EEG and nocturnal secretory activity of growth hormone (GH) and cortisol were evaluated. The lower dosage was administered to four subjects and the higher dosage to eight on 5 consecutive days, preceded and followed by 2 days of placebo treatment. After 25 mg of tropisetron, there was a slight increase in REM sleep in the first part of the sleep period, and stage 2 was decreased during the total night.

Growth hormone-releasing hormone (GHRH)-induced effects on sleep EEG and nocturnal secretion of growth hormone, cortisol and ACTH in patients with major depression.

Studies in normal human subjects and animals suggest that the neuropeptide growth hormone-releasing hormone (GHRH) is a common regulator of the sleep EEG and nocturnal hormone secretion. In healthy volunteers GHRH prompts an increase in the amount of slow wave sleep (SWS) and in growth hormone (GH) secretion and blunting of cortisol release. Inhibition of GHRH may contribute to sleep-endocrine aberrances during depression.

Flumazenil exerts intrinsic activity on sleep EEG and nocturnal hormone secretion in normal controls.

The physiological function of benzodiazepine (BDZ) receptors includes regulation of sleep and neuroendocrine activity. Most of the pharmacological effects of BDZ are blocked by flumazenil. However, recent neurological and behavioral studies suggest that flumazenil has its own central intrinsic activity.

Effects of long-term treatment with the MAO-A inhibitor moclobemide on sleep EEG and nocturnal hormonal secretion in normal men.

Sleep EEG, nocturnal penile tumescence (NPT) and nocturnal hormone secretion were studied in four normal males during placebo, under up to 300 mg per day of moclobemide, the short-acting and reversible inhibitor of monoamine oxidase (type A), and after withdrawal. Under moclobemide, REM sleep was slightly suppressed. Drug cessation was followed by REM rebound.

Neurosteroid pregnenolone induces sleep-EEG changes in man compatible with inverse agonistic GABAA-receptor modulation.

The steroid pregnenolone (P) and its sulfate (PS) can accumulate in the central nervous system independent of peripheral sources. Pharmacologically, the sulphated form of P interacts with the GABAA receptor complex, and functional assays show that this steroid behaves as an allosteric GABAA receptor antagonist. The present study explored the effect of a single dose of P upon the sleep-EEG and concurrent secretion of growth hormone and cortisol in male volunteers.

Functional properties of deoxycorticosterone and spironolactone: molecular characterization and effects on sleep-endocrine activity.

Adrenal steroid hormones are capable of interfering with a variety of behavioral phenomena including sleep. The mechanisms appear to involve effects at the cell membrane as well as nuclear actions mediated by intracellular mineralo- and glucocorticosteroid receptors (MR and GR). We employed the MR agonist deoxycorticosterone (DOC) and the MR antagonist spironolactone (SP) to study the role of MRs in the regulation of human sleep.

Differential effects of the enantiomers R(-) and S(+) oxaprotiline on major endogenous depression, the sleep EEG and neuroendocrine secretion: studies on depressed patients and normal controls.

The effects of the optically active enantiomers of oxaprotiline (OXP), R(-) OXP and S(+) OXP, on depressive symptomatology and the sleep EEG were investigated in two separate exploratory studies. In addition, the neuroendocrine profile of both compounds was characterized in normal controls. In the patients treated with a daily oral dose of 150 mg S(+) OXP we found a Hamilton depression score that decreased from 29.

Studies of nocturnal penile tumescence and sleep electroencephalogram in patients with major depression and in normal controls.

Nocturnal penile tumescence (NPT), sleep electroencephalogram and testosterone secretion were investigated in 25 nonmedicated male patients with an acute episode of major depression. Twelve patients were reassessed after a stable remission and withdrawal of antidepressants. Four of the 25 patients had no NPT activity during acute depression, but this was reversed after recovery.

The sleep EEG and nocturnal hormonal secretion studies on changes during the course of depression and on effects of CNS-active drugs.

1. The sleep EEG and nocturnal hormone secretion were studied simultaneously in normal male controls and in male patients with major endogenous depression before treatment with tricyclics and after recovery and drug cessation. 2.

Sleep EEG effects of 3,4-methylenedioxyethamphetamine (MDE; "eve") in healthy volunteers.

3,4-methylenedioxyethamphetamine (MDE; "Eve") exerts similar psychotropic effects in humans as 3,4-methylenedioxymethamphetamine (MDMA; "Ecstasy") and is less toxic in animal studies. We conducted a double-blind, placebo-controlled, cross-over sleep electroencephalogram (EEG) study with healthy volunteers. One hundred forty milligrams of MDE or placebo were administered PO in six subjects at 11 PM.

Effects of growth hormone-releasing hormone and somatostatin on sleep EEG and nocturnal hormone secretion in male controls.

When applied centrally to animals, growth hormone-releasing hormone (GHRH) stimulates slow-wave sleep (SWS), whereas somatostatin (SRIF) increases REM sleep. We investigated whether these peptides also affect the sleep EEG in humans when given intravenously by comparing polysomnographically the effects of four boluses of (1) placebo, (2) 50 micrograms GHRH or (3) 50 micrograms SRIF administered at 22.00, 23.

Studies on geranylgeranyl diphosphate synthase from rat liver: specific inhibition by 3-azageranylgeranyl diphosphate.

Geranylgeranyl diphosphate synthase from rat liver was separated from farnesyl diphosphate synthase, the most abundant and widely occurring prenyltransferase, by DEAE-Toyopearl column chromatography. The enzyme catalyzed the formation of E,E,E-geranylgeranyl diphosphate (V) from isopentenyl diphosphate (II) and dimethylallyl diphosphate (I), geranyl diphosphate (III), or farnesyl diphosphate (IV) with relative velocities of 0.09:0.

[The importance of applied ethology for the execution of animal welfare legislation].

Applied ethology in general and farm animal ethology in particular have a great importance in connection with animal welfare regulations on a national and international level. They have through the legislation on animal welfare brought about important repercussions on housing of farm animals, wild animals and experimental animals in Switzerland. The animal welfare legislation has been a considerable boost to scientific research.

Effects of an ACTH/MSH(4-9) analog (HOE 427) on the sleep EEG and nocturnal hormonal secretion in humans.

The synthetic ACTH/MSH(4-9) analog HOE 427 ("ebiratide"), which is behaviorally the most potent ACTH-derived peptide but which is devoid of endocrine activity, was administered intravenously in a pulsatile mode 4 times (120 micrograms each) at 2200, 2300, 2400 and 0100 to study its effect on the sleep EEG and on concomitant hormonal secretion of cortisol and growth hormone. In comparison to placebo, the peptide produced signs of general activation associated with specific deteriorating effects on the quality of sleep. Sleep onset latency and intermittent wakefulness were increased, slow wave sleep was reduced, but only during the first 3 hours of the sleep period.

Sleep EEG and nocturnal secretion of testosterone and cortisol in patients with major endogenous depression during acute phase and after remission.

Sleep EEG and the nocturnal secretion of cortisol and testosterone in 12 male patients (mean age 46.4 +/- 11.26 years) with major endogenous depression were investigated concomitantly during acute depression, before treatment and after recovery and drug cessation.

Examination and treatment of sleep-related painful erections--a case report.

The case of a patient with sleep-related painful erections is described. Insomnia and a slight depressive syndrome occurred along with a long history of this disorder. No physical abnormality was found.

Sleep EEG and nocturnal secretion of cortisol and growth hormone in male patients with endogenous depression before treatment and after recovery.

The authors conducted a sleep-endocrine evaluation among 10 unmedicated male patients with major endogenous depression during their depressive episode and following full clinical remission and drug withdrawal. While abnormally high values for cortisol secretory activity normalized after return to euthymia, growth hormone release and characteristic disturbances of EEG sleep remained unchanged. Whether or not neuroendocrine and sleep EEG abnormalities, which are present in remission, are trait markers remains undecided until premorbid sleep-endocrine data are available.

[Animal welfare legislation and animal experiments in Switzerland--effects and challenges].

The Swiss animal welfare legislation, which restricts experiments on animals, entered into force in 1981. The discussions, the legal prescriptions, the official guidelines and the ethical principles for animal experimentation issued by scientists are treated. The legislation has slowly brought about positive effects.

Effects of fluoxetine upon pharmacoendocrine and sleep-EEG parameters in normal controls.

A single dose of 80 mg fluoxetine induced a slight increase in cortisol secretion when compared to placebo in an acute endocrine challenge test including assessment of prolactin, growth hormone, luteinizing hormone, follicle stimulating hormone, testosterone. This pretreatment with 80 mg fluoxetine did not change the ACTH release after blockade of the feed-back regulation of peripheral corticosteroids on ACTH secretion by metyrapone. Sleep-EEG revealed reduction of rapid-eye-movement sleep.

Effects of trimipramine on sleep EEG, penile tumescence and nocturnal hormonal secretion. A long-term study in 3 normal controls.

Sleep EEG, nocturnal penile tumescence (NPT) and nocturnal endocrine activity were studied in 3 male control subjects during placebo, under trimipramine (TR) and after withdrawal. TR did not change the sleep structure. NPT activity tended to increase under TR.

Effects of clomipramine on sleep EEG and nocturnal penile tumescence: a long-term study in a healthy man.

The effects of the tricyclic antidepressant clomipramine on sleep EEG and nocturnal penile tumescence (NPT) were investigated during a long-term study in a normal male control subject. During 21 consecutive days the subject received first placebo for 3 days, then stepwise increasing dosages of clomipramine for 10 days, and finally placebo after withdrawal for 8 days. Under clomipramine, rapid eye movement (REM) sleep was suppressed markedly; an REM rebound occurred after withdrawal.