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M Opp

Publications and source records attributed to M Opp.

13 recordsLinked to original sources
PubMed1994

Involvement of prolactin in the REM sleep-promoting activity of systemic vasoactive intestinal peptide (VIP).

The involvement of pituitary prolactin (PRL) in systemic vasoactive intestinal peptide (VIP)-induced sleep was studied. Male rats were implanted with electrodes for EEG-recording, with brain thermistors to record cortical temperature (Tcrt) and with chronic intracardial catheters to obtain blood samples and to deliver substances. One group of rats (n = 8) received normal rabbit serum (NS)+physiological saline (SAL) on the baseline day and was injected with NS+VIP on the experimental day. In the other group of rats (n = 6), the baseline day was followed by administration of PRL-antiserum (PRL-AS) + VIP on the experimental day. The sera and VIP or SAL were injected 30 min before and at light onset, respectively. Sleep-wake activity was then recorded for the next 12-h light period. Systemic VIP-stimulated PRL secretion as measured by RIA in serial samples obtained hour 1 postinjection. VIP also elicited selective increases in REM sleep (REMS) in the rats pretreated with NS. Tcrt was not affected by VIP. Administration of PRL-AS blocked the increase in circulating levels of free (non-IgG-bound) PRL and prevented VIP-enhanced REMS. Comparisons of the sleep effects of PRL-AS+VIP with the previously reported changes in sleep after PRL-AS alone indicate that PRL has a major role in the mediation of the REMS-promoting activity of systemic VIP. The results suggest that an increased release of endogenous pituitary PRL modulates REMS.

Animals↗
PubMed1992

Growth hormone-releasing hormone antibodies suppress sleep and prevent enhancement of sleep after sleep deprivation.

Previous reports suggest that the hypothalamic growth hormone-releasing hormone (GHRH) promotes sleep, especially non-rapid-eye-movement sleep (NREMS). To evaluate the role of endogenous GHRH in sleep regulation, the effects of antibodies to rat GHRH (GHRH-ab) were studied on normal sleep, brain temperature (Tbr), and GH secretion in experiment I and on enhanced sleep after sleep deprivation in experiment II. In experiment I, affinity-purified GHRH-ab (50 and 200 micrograms) raised in goats and a control goat immunoglobulin G (IgG) preparation were injected intracerebroventricularly (icv) in rats 1 h before the onset of the light cycle, and sleep-wake activity and Tbr were recorded for the next 12 or 23 h. Both doses of GHRH-ab suppressed NREMS and REMS throughout the light cycle. Sleep durations at night were normal. Electroencephalographic (EEG) slow-wave activity, characterized by EEG slow-wave amplitudes, was reduced after GHRH-ab during both the light and the dark cycles. Plasma GH concentrations measured 6-12 h after injection of GHRH-ab (200 micrograms) were diminished. Both the control IgG and GHRH-ab elicited fever. In experiment II, the sleep-wake activity and Tbr of rats were recorded for 24 h in three experimental conditions: base-line with icv injection of IgG, 3-h sleep deprivation with icv IgG injection, and 3-h sleep deprivation with icv GHRH-ab (200 micrograms). After sleep deprivation (+IgG), a prompt increase in EEG slow-wave activity (power density analysis) and late increases in NREMS and REMS durations were found.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Inhibition of growth hormone-releasing factor suppresses both sleep and growth hormone secretion in the rat.

To study the possible involvement of hypothalamic growth hormone-releasing factor (GRF) in sleep regulation, a competitive GRF-antagonist, the peptide (N-Ac-Tyr1,D-Arg2)-GRF(1-29)-NH2, was intracerebroventricularly injected into rats (0.003, 0.3, and 14 nmol), and the EEG and brain temperature were recorded for 12 h during the light cycle of the day. Growth hormone (GH) concentrations were determined from plasma samples taken at 20-min intervals for 3 h after 14 nmol GRF-antagonist. The onset of non-rapid eye movement sleep (NREMS) was delayed in response to 0.3 and 14 nmol GRF-antagonist, the duration of NREMS was decreased for one or more hours and after 14 nmol EEG slow wave amplitudes were decreased during NREMS in postinjection hour 1. The high dose of GRF-antagonist also suppressed REMS for 4 h, inhibited GH secretion, and elicited a slight biphasic variation in brain temperature. These findings, together with previous observations indicating a sleep-promoting effect for GRF, support the hypothesis that hypothalamic GRF is involved in sleep regulation and might be responsible for the correlation between NREMS and GH secretion reported in various species.

Animals↗
PubMed1991

Sleep in diabetic rats: effects of interleukin 1.

Previous observations indicate that both interleukin 1 beta (IL-1 beta) and insulin are involved in sleep regulation. IL-1 beta has been reported to stimulate insulin secretion, suggesting that some of the effects of IL-1 beta are mediated by insulin. The purpose of the current experiments was to study the possible role of endogenous insulin in physiological sleep regulation and in the hypnogenic effects of exogenously administered IL-1 beta. Isotonic saline or IL-1 beta (2.5 ng) was intracerebroventricularly injected into normal and streptozocin-diabetic rats at dark onset, and sleep-wake activity and brain temperature were recorded for 24 h. Blood samples were collected every 20 min during the first hour postinjection for plasma insulin measurement. In diabetic rats, rapid-eye-movement (REM) and non-REM sleep were significantly decreased during the second part of the light period on the baseline day. IL-1 beta elicited a biphasic sleep response in both normal and diabetic rats. This initial increase in non-REM sleep during the first 4 h postinjection was followed by significant sleep suppression in both groups. Brain temperature was not affected in either group. Plasma insulin concentration decreased in response to IL-1 beta in normal rats, whereas insulin was below the level of detection in the diabetic rats. These results indicate that, although sleep is disturbed in diabetic rats, pancreatic insulin might not have a decisive role in the regulation of sleep in rats, and it does not mediate the effects of IL-1 beta on sleep-wake activity.

Animals↗
PubMed1990

Interleukin 1 alpha and an interleukin 1 beta fragment are somnogenic.

The somnogenic activity of interleukin 1 beta (IL-1 beta) has previously been established. Interleukin 1 alpha (IL-1 alpha) is a distinct gene product that possesses similar biological activities. We report here that IL-1 alpha, like IL-1 beta, has the capacity in rabbits to enhance non-rapid-eye-movement sleep, electroencephalographic slow-wave (0.5-3.5 Hz) voltages, and body temperatures and to inhibit rapid-eye-movement sleep. After IL-1 alpha, sleep remained episodic, and at the doses used no abnormal behavior was observed. Several synthetic IL-1 alpha and IL-1 beta peptides were also tested in vivo for somnogenic and pyrogenic activity and in vitro for their ability to stimulate prostaglandin E2 (PGE2) production by fibroblasts and proliferation of T-cells. Only IL-1 beta-(208-240) enhanced non-rapid-eye-movement sleep and body temperature, although both IL-1 beta-(208-240) and IL-1 alpha-(223-250) stimulated PGE2 production; both of these peptides failed to stimulate T-cell production. In contrast, four other IL-1 peptides were nonpyrogenic and somnogenically inactive yet stimulated T-cell proliferation. We conclude that the components of IL-1 required for sleep and temperature activities are different from those required for T-cell proliferation.

Animals↗
PubMed1989

Prolactin, vasoactive intestinal peptide, and peptide histidine methionine elicit selective increases in REM sleep in rabbits.

The purpose of these experiments was to determine whether (1) vasoactive intestinal peptide (VIP) produces effects on rabbit sleep similar to those reported for rats and cats; (2) peptide histidine methionine (PHM), a peptide closely related to VIP, mimics the sleep effects of VIP; and (3) pituitary prolactin (PRL), a pituitary hormone that has a sleep-related secretory pattern and for which VIP and PHM act as releasing factors, has similar effects on sleep. VIP or PHM (0.01, 0.1 and 1.0 nmol/kg) was intracerebroventricularly (i.c.v.) injected; PRL (ovine PRL, 45 and 200 IU/kg) was subcutaneously (s.c.) administered. Sleep-wake activity and brain temperature were recorded for 6 h. For controls, rabbits received artificial cerebrospinal fluid i.c.v. or PRL-vehicle s.c. VIP and PHM promoted rapid eye movement sleep (REMS), although these effects were not dose-dependent. In addition, the high dose of VIP and PHM transiently increased wakefulness. Increases in REMS occurred only during hours 2-6 after i.c.v. injection of VIP and peptide histidine leucine (PHI). After s.c. injection of PRL, REMS started to increase in postinjection hour 3. The effect of the high dose was significantly more pronounced than that of the small dose. Each substance enhanced the frequency of REMS episodes, and the high dose of PRL also increased the duration of REMS bouts. These results are consistent with the hypothesis that VIP is involved in physiological regulation of REMS, and that the VIP- and PHM-induced increases in REMS may be mediated via release of PRL.

Animals↗
PubMed1989

Interleukin-6 is pyrogenic but not somnogenic.

Interleukin-6 (IL6) induces acute phase protein production and is hypothesized to mediate systemic and central effects of IL1. To determine whether IL6 possesses somnogenic properties, rabbits were injected intracerebroventricularly with IL6; sleep-wake activity was determined and brain temperatures recorded for 6 hr. IL6 induced fever in a dose-related manner with no effect on sleep-wake activity. IL6, therefore, is the first cytokine reported to elicit fever without promoting sleep. We conclude that the somnogenic action of IL1 is not mediated through IL6.

Acute-Phase Proteins↗
PubMed1989

Corticotropin-releasing factor attenuates interleukin 1-induced sleep and fever in rabbits.

Interleukin 1 (IL-1), a key mediator of the acute phase response, stimulates hypothalamic corticotropin-releasing factor (CRF) release. The CRF-adrenocorticotrophic hormone (ACTH)-glucocorticoid axis is a feedback for peripheral production and action of IL-1. Effects of intracerebroventricularly administered CRF on rabbit sleepwake activity, brain temperature (Tbr), and behavior and on the central effects of IL-1 [fever and excess non-rapid-eye-movement sleep (NREMS)] were studied. CRF (0.1-1.25 micrograms) dose dependently decreased NREMS and enhanced wakefulness. IL-1-induced excess NREMS was inhibited by CRF. Rapid-eye-movement sleep (REMS) suppressed by IL-1 was partially restored by 0.1 or 0.5 microgram CRF, although CRF itself did not promote REMS. Behavioral effects of intracerebroventricular CRF were relatively small, although 1.25 micrograms abolished ingestion for 3 h, suppressed rearing behavior, and increased sitting behavior. Tbr increased after CRF injection alone. After IL-1 pretreatment, however, 0.1 and 0.5, but not 1.25, micrograms CRF reduced IL-1-induced fever after several hours. These results implicate IL-1-induced CRF release as part of a negative-feedback mechanism attenuating not only peripheral IL-1 actions but also its central effects.

Animals↗
PubMed1978

Pulling the plug.

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Ethics Committees, Clinical↗
PubMedDate not supplied

Laboratory diagnosis of congenital human cytomegalovirus infection using polymerase chain reaction and shell vial culture.

Congenital HCMV infection was diagnosed at the 22th week of gestation. The infection was suspected because HCMV IgM was detected in a serum sample obtained from the woman's husband. HCMV infection was detected in the amniotic fluid by polymerase chain reaction, shell vial culture (immunoperoxidase assay) and conventional virus isolation. Serologic testing in paired sera of the woman and in umbilical cord blood for specific IgM and IgA remained negative. As serological data (preconceptional HCMV serostatus) were incomplete, a clear differentiation between primary and secondary infection could not be achieved; consequently, risk quantification could not be determined. Viruria was detected in the offspring during the 1st week post partum. No clinical signs of cytomegalic inclusion disease were diagnosed up to six weeks post partum. Our case report indicates that for pregnancy surveillance, serologic testing for HCMV antibody should also be performed in the spouse.

Adult↗
PubMedDate not supplied

Somnogenic cytokines and models concerning their effects on sleep.

All the sleep-promoting substances currently identified also have other biological activities. Despite years of effort, a single specific central nervous system sleep center has not been described. These observations led us to propose a biochemical model of a sleep activational system in which the effects of several sleep factors are integrated into a regulatory scheme. These sleep factors interact by altering the metabolism, production, or activity of each other and thereby result in multiple feedback loops. This web of interactions leads to sleep stability in that minor challenges to the system will not greatly alter sleep. The system, however, is responsive to strong perturbations, such as sleep deprivation and infectious disease. The sleep-promoting effects of cytokines and their interactions with prostaglandins and the neuroendocrine system are used to illustrate the functioning of a part of the sleep activational system under normal conditions and during infectious disease. Although the actions of individuals sleep factors are not specific to sleep, their interactions at various levels of the neuraxis can mediate a specific sleep response. Such a system would also be responsive to the autonomic and environmental parameters that alter sleep.

Animals↗