Effects of prolactin on sleep in cyclic rats

We previously demonstrated that pregnancy-associated sleep enhancement is correlated with the daily surges of prolactin (PRL). However, in spite of a surge of PRL in the proestrous night, a reduction of nocturnal sleep occurs in phase with proestrus. Therefore, to clarify the physiological role of PRL in sleep regulation during the estrous cycle, time-course changes in sleep were analyzed in bromocriptine (CB-154)-treated and/or PRL-supplemented female rats. Sleep patterns characteristic of proestrus-to-estrus were not affected by the CB-154 treatment. In contrast, nocturnal rapid eye movement sleep (REMS) was significantly increased after the PRL supplementation. The CB-154 treatment diminished the REMS-enhancing effect of PRL. Thus, the results suggest that the endogenous PRL is not crucial for the regulation of sleep during the estrous cycle, while exogenous PRL can enhance REMS.     

The involvement of serotonin neurones in the inhibition of renal nerve activity during desynchronized sleep

Numerous 5-hydroxytryptamine (5-HT)-containing cell bodies were visualized by fluorescence microscopy in the caudal brainstem rostal to the decussation of the pyramids in a region from which a desynchronized sleep-like pattern of sympathetic activity was obtained in a previous study. In unanaesthetized mid-collicular decerebrated cats recordings were made of sympathetic activity in a renal nerve. The inhibition of renal nerve activity occurring during desynchronized sleep-like state induced by physostigmine was attenuated significantly by procedures which interfered with the pathways from the 5-HT-containing neurones. Small cuts in the dorsolateral funiculus of the cervical spinal cord reduced the inhibition from43 ± 6%to14.0 ± 3%. Microinjection of 5,7-dihydroxytryptamine into cervical spinal cord reduced the serotonin content of the thoracic cord by 22.4% and attenuated the desynchronized sleep-like state inhibition of renal nerve activity by a similar amount. Depletion of serotonin withp-chlorophenylalanine significantly reduced the inhibition of renal nerve activity during the desynchronized sleep-like state, from42.5 ± 5%to10.0 ± 2.0%. It was suggested that serotonin-containing neurones are likely to be involved in the inhibition of renal nerve activity occurring during desynchronized sleep.     

Possible involvement of serotonergic neurons in the reduction of locomotor hyperactivity caused by amphetamine in neonatal rats depleted of brain dopamine

This experiment attempted to determine the mechanism by which amphetamine reduces locomotor hyperactivity in neonatal rats given brain dopamine (DA)-depleting 6-hydroxydopamine (6-OHDA) injections. Brain DA neurons were destroyed selectively in neonatal rats by intraventricular (i.v.t.) injections of 6-OHDA following desmethylimipramine (DMI) pretreatment. Control rats received DMI and i.v.t. injections of the 6-OHDA vehicle solution. Rats given the 6-OHDA treatment displayed 7-fold increases in locomotor activity compared to controls during days 16–55 of life. Throughout this period, amphetamine (1 mg/kg) reduced locomotor hyperactivity in 6-OHDA-treated rats but increased locomotor activity in control rats. The reduction of hyperactivity caused by amphetamine (0.5–4 mg/kg) was dose-related and was not accompanied by stereotyped behavior. Like amphetamine, methylphenidate (4 mg/kg) reduced locomotor hyperactivity in rats given 6-OHDA. The DA antagonist, spiroperidol (50–200 μg/kg) failed to attenuate the hyperactivity-reducing effect of amphetamine in 6-OHDA-treated rats at doses which abolished the stimulant effect of amphetamine in control rats. However, the serotonin antagonist methysergide (0.5–4 mg/kg) produced dose-dependent antagonism of the effect of amphetamine in 6-OHDA-treated rats. Pretreatment with propranolol (5 mg/kg), phentolamine (5 mg/kg), atropine (0.5 mg/kg) or naloxone (10 mg/kg) failed to alter the reduction in locomotor hyperactivity caused by amphetamine. The serotonin releasing agent, fenfluramine (3 mg/kg), and the serotonin agonist, quipazine (0.5–4 mg/kg), both reduced locomotor hyperactivity in 6-OHDA-treated rats while not altering locomotion in control rats. These results confirm previous observations that amphetamine reduces locomotor hyperactivity caused by neonatal 6-OHDA administration and suggest that this effect is mediated by increased serotonergic neurotransmission.     

Parental rating of sleep in children with attention deficit/hyperactivity disorder

Objective  Sleep problems have often been associated with attention deficit/hyperactivity disorder (ADHD). Parents of those with ADHD and children with ADHD report sleep difficulties more frequently than healthy children and their parents. The primary objective of this paper is to describe sleep patterns and problems of 5 to 11-year-old children suffering from ADHD as described by parental reports and sleep questionnaires. Method  The study included 321 children aged 5–11 years (average age 8.4 years); 45 were diagnosed with ADHD, 64 had other psychiatric diagnoses, and 212 were healthy. One hundred and ninety-six of the test subjects were boys and 125 were girls. A semi-structured interview (Kiddie-SADS-PL) was used to DSM-IV diagnose ADHD and comorbidity in the clinical group. Sleep difficulties were rated using a structured sleep questionnaire (Children Sleep Behaviour Scale). Results  Children diagnosed with ADHD had a significantly increased occurrence of sleep problems. Difficulties relating to bedtime and unsettled sleep were significantly more frequent in the ADHD group than in the other groups. Children with ADHD showed prolonged sleep onset latency, but no difference was shown regarding numbers of awakenings per night and total sleep time per night. Comorbid oppositional defiant disorder appeared not to have an added effect on problematic behaviour around bedtime. Conclusion  Parents of children with ADHD report that their children do not sleep properly more often than other parents. The ADHD group report problems with bedtime resistance, problems with sleep onset latency, unsettled sleep and nightmares more often than the control groups. It may therefore be relevant for clinicians to initiate a closer examination of those cases reporting sleep difficulties.     

Effects of pontine lesions on brain stem polyneuronal activity during sleep in infant rats

Multiple-unit activity was recorded from residual neurons in the gigantocellular field (FTG) of the pontine reticular formation in young rats after extensive contralateral FTG lesions. Epochs of normal appearing active sleep continued to occur but were characterized by abnormally low FTG neuronal firing rates. In contrast, during epochs of active sleep with exaggerated motility, the FTG discharge frequencies approximated those observed during active wakefulness.     

Quipazine has a biphasic effect on slow wave sleep and reduces REM sleep rebound in REM sleep deprived rats

Rats implanted with electrodes for polygraphic recording were deprived of REM sleep for 24 hr. Following REM sleep deprivation animals were injected with quipazine maleate (7.5 mg/kg IP) and were polygraphically recorded for 48 hr. The results show that quipazine reduces REM sleep rebound and that it has a biphasic effect on slow-wave sleep: initial 6 hr suppression is followed by a delayed increase in the second 24 hr recording period. The initial suppression of slow-wave sleep we attribute to the stimulation of central serotonergic receptors while the effect on REM sleep rebound may result from quipazine's action on central catecholamines.     

Changes in serotonin in rat brain during slow-wave sleep and paradoxical sleep: application of the microwave fixation method to sleep research

Neural responses to several chemicals of the pit organs and terminal buds on the facial skin of the carp were compared electrophysiologically. Nerve inpulses from the pit organs were larger than those from the terminal buds. The pit organs were more sensitive to salts and especially acids than the terminal buds. The former did not respond to sucrose, silk worm pupa extract, betaine and amino acids except acidic ones. The latter, however, responded well to them.     

Effects of early handling on basal and stress-induced sleep parameters in rats

Exposure of humans and animals to stressful events early in life leads to significant and often permanent behavioural, neuroendocrine and central alterations. Early handling consists of removing the litter from the nest for 15 min/day, from post-natal days 2 to 14 and results in lowered ACTH and corticosterone stress response and reduced anxiety-like and fear behaviours. Stress-induced sleep alterations usually consists of increased sleep time, known as sleep rebound. In the present study, basal and stress-induced sleep pattern of control non-manipulated (CTL) and early handled (EH) adult male rats was investigated. Sleep was evaluated by 21-h polysomnographic recordings (from 10:00 to 07:00 h of the next day) before and after a 1-h session of restraint stress. The results showed that in the first 3 h following stress, both CTL and EH animals exhibited an impairment of sleep, with a reduction of sleep efficiency, duration of slow wave sleep and of paradoxical sleep. On the contrary, time awake and awakening bouts were augmented in this period. Sleep rebound was observed mainly in the dark period of the light-dark cycle. Stress-induced sleep changes were similar between CTL and EH animals for most sleep parameters. However, EH animals exhibited more bouts of paradoxical sleep on the night following stress exposure and longer bouts of paradoxical sleep in the light period that followed restraint stress. These data indicate that stress-induced alterations of sleep in early handled animals are similar to that observed in control animals, except for some parameters related to paradoxical sleep.     

Cocaine-induced genital reflexes in paradoxical sleep deprived rats: Indications of mediation by serotonin receptors

As paradoxical sleep deprivation (PSD) modifies cocaine-induced genital reflexes (penile erection [PE] and ejaculation [EJ]) and since cocaine is a serotonin (5-HT) reuptake inhibitor, we hypothesized that 5-HT also plays a role in these genital reflexes in PSD male rats. After a 4-day period of PSD each group was administered with serotonergic drugs prior to cocaine and placed in observation cages. The selective 5-HT(1) agonist (8-OH-DPAT) completely abolished PE events whereas the antagonist (pindolol) did not produce significant effects in the number of animals displaying PE. It was found that both drugs reduce the frequency of PE. There were no significant effects on the number of animals that ejaculated or in its frequency after pindolol although both parameters were reduced by the agonist at the highest doses (2 and 4 mg/kg, SC). Pretreatment with the 5-HT(2) agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) (0.12; 0.5 and 1 mg/kg, SC) significantly reduced the number of rats displaying PE and all doses reduced both PE and EJ frequencies. The number of animals displaying PE after 5-HT(2) antagonist (ketanserin) pretreatment at 1 and 2.5 mg/kg doses was significantly decreased in relation to vehicle rats and all doses reduced PE frequency. 5-HT(2) compounds at any dose did not affect the number of animals ejaculating, but the frequency was significantly reduced by all doses of DOI and by 1 to 5 mg/kg doses of ketanserin. Taken together, the results suggest that serotonergic receptors play an important role in genital reflexes induced by cocaine in sleep deprived males.     

Effects of prolactin-releasing peptide (PrRP) on sleep regulation in rats

The present study examined in rats how prolactin-releasing peptide (PrRP), a new hypothalamic hormone, infused centrally during the dark period affects sleep and plasma levels of prolactin (PRL). At a dose of 0.1 nmol, PrRP increased only rapid eye movement (REM) sleep, whereas with 1.0 nmol both non-REM sleep and REM sleep were enhanced. However, 10.0 nmol of PrRP increased only non-REM sleep with a febrile response. The levels of plasma PRL were elevated during the infusion of PrRP with 0.1 and 1.0 nmol. Consequently, the increased release of PRL correlated with significant increases in REM sleep, but not in non-REM sleep.     

Effects of different sleep deprivation protocols on sleep perception in healthy volunteers

Objectives

To investigate whether different protocols of sleep deprivation modify sleep perception.

Methods

The effects of total sleep deprivation (TD) and selective rapid eye movement (REM) sleep deprivation (RD) on sleep perception were analyzed in normal volunteers. Thirty-one healthy males with normal sleep were randomized to one of three conditions: (i) normal uninterrupted sleep; (ii) four nights of RD; or (iii) two nights of TD. Morning perception of total sleep time was evaluated for each condition. Sleep perception was estimated using total sleep time (in hours) as perceived by the volunteer divided by the total sleep time (in hours) measured by polysomnography (PSG). The final value of this calculation was defined as the perception index (PI).

Results

There were no significant differences among the three groups of volunteers in the total sleep time measured by PSG or in the perception of total sleep time at baseline condition. Volunteers submitted to RD exhibited lower sleep PI scores as compared with controls during the sleep deprivation period (P < 0.05). Both RD and TD groups showed PI similar to controls during the recovery period.

Conclusion

Selective REM sleep deprivation reduced the ability of healthy young volunteers to perceive their total sleep time when compared with time measured by PSG. The data reinforce the influence of sleep deprivation on sleep perception.     

Effects of aniracetam on impaired sleep patterns in stroke-prone spontaneously hypertensive rats

The aim of the present study was to determine the pattern of sleep disturbances and the effects on sleep of aniracetam, a cognitive enhancer, in stroke-prone spontaneously hypertensive rats (SHRSP). Compared with normotensive control rats, SHRSP exhibited an impaired sleep pattern characterized by suppressed diurnal rapid eye movement (REM) sleep and excessive nocturnal non-REM sleep. At a dose of 30 mg/kg per day p.o., aniracetam increased REM sleep in the light period after administration for 5 consecutive days. Consequently, suppressed REM sleep in SHRSP was restored by repeated treatment with aniracetam. Aniracetam could be useful in improving REM sleep impairment associated with vascular dementia.     

Effects of the timing of exercise on the night sleep

Abstract The effects of physical exercises taken at different times in the day upon subjective sleep feeling were examined in five healthy university students (aged 20–22 years); morning exercise, evening exercise, and late evening exercise. The late evening exercise with the strength of 50–60% VO₂max of 1 h has the effect of getting better subjective sleep feeling in the morning and the effect of the decreased daytime sleepiness.     

大鼠睡眠剥夺方法的研究进展

目前睡眠的功能并不十分清楚．睡眠研究方法的不足很大程度上制约了睡眠研究及其理论的发展。睡眠剥夺是目前一种很有发展潜力的研究睡眠的手段．它对人们研究睡眠各期的功能有很强的启发性。在睡眠剥夺研究中．要想得到可靠的实验结果．需要有效专一地消除睡眠，因而，消除睡眠的睡眠剥夺方法在研究中有着很重要的意义。本文将几种常用的大鼠睡眠剥夺方法予以综述．     

Effects of melatonin and propranolol on sleep of the rat

Melatonin and l-propranolol, which inhibits melatonin synthesis, were administered to rats at 07.45 h and 19.45 h. Melatonin given in the morning decreased non-REM sleep, but when given at night had no effect on sleep stages. l-propranolol given in the morning had no effect on non-REM sleep, but increased it at night. l-propranolol produced decreased in percentage REM sleep at both times.     

Effects of isoflurane and ketamine on sleep in rabbits.

The postoperative sleep disturbance (POSD) is characterized by reduction of sleep after surgical operation. However, its mechanism is not well known. Therefore, we hypothesized that anesthetics could contribute to the POSD, and studied the effects of isoflurane and ketamine on sleep in rabbits. Rabbit sleep was measured for 21 h after isoflurane exposure or intravenous injection of ketamine. Non-rapid eye movement sleep (NREMS) was decreased after isoflurane anesthesia. In contrast, ketamine anesthesia significantly enhanced NREMS. Both anesthetics did not affect rapid eye movement sleep. These results suggest that isoflurane may contribute to the POSD, but ketamine may decrease the POSD.