Electrodes For Sleep Recordings Research Articles

Nicotine and fluoxetine induce arousing effects on sleep–wake cycle in antidepressive doses: A possible mechanism of antidepressant-like effects of nicotine

A number of studies have reported an association between smoking and depression, and several reports suggest that nicotine (NIC) may act as an antidepressant. The present study was designed to determine whether the effects of NIC on sleep–wake patterns in rats are similar to those of the antidepressant fluoxetine (FLX), a selective serotonin reuptake inhibitor. Male rats were chronically implanted with a standard set of electrodes for sleep recording. We compared the effects of antidepressive doses of NIC, FLX and the combination of both drugs on sleep–wake pattern in rats subjected to one day, one week and two weeks of administration, as well as after the withdrawal of the two-week treatment. The changes observed in our study in an 8-h sleep recording period during one day, one week and two weeks of NIC administration are very similar to those observed in the rats that received FLX, which led to a decrease in both slow wave sleep II and rapid eye movement (REM) sleep as a consequence of an increase in wakefulness. In addition, all treatments also induced a significant lengthening of REM sleep latency onset. These data suggest that the antidepressant-like action of NIC could be caused by its arousing properties.

Effects of selective dopamine D4 receptor antagonist, L-741,741, on sleep and wakefulness in the rat

The influence of the dopamine system upon sleep/wake states is not fully understood. To date, the role of dopamine D4 receptor has not been studied. The aim of this work is to study the influence of dopamine D4 receptor upon sleep/wake states in male rats. Male Wistar rats were implanted with electroencephalography and electromyography electrodes for sleep recording. Sleep/wake times were compared in rats first treated with control solution (vehicle) and the day after treated with a potent and highly selective D4 dopamine receptor antagonist. L-741,741 (1.5, 3, 6 mg/kg) or vehicle solution (10% DMSO in saline) was administered intraperitoneally at the beginning of the light period. Subsequently, 3 h of polysomnography were recorded and sleep–wake parameters evaluated. For statistical comparisons, Wilcoxon ranges test was performed. L-741,741 (1.5 mg/kg) only increased Light Slow Wave Sleep (SWS). 3 mg/kg enhanced Quiet Waking (QW) increasing number of episodes, whereas Active Waking (AW) was reduced decreasing mean episode duration. 6 mg/kg reduced number of episodes of Deep SWS and increased its latency. Light SWS was decreased reducing number of episodes and their duration. Total time spent asleep was reduced and time spent in AW was increased. REM latency was increased. These results suggest a role for D4 receptors in the regulation of wake and sleep.

Anesthésie locorégionale pour la chirurgie de la main

This study aimed to test the hypothesis that, during extended wakefulness, parasympathetic activity is associated with the depth of the subsequent recovery sleep in mice. Fourteen male C57BL/6 mice were implanted with electrodes for sleep recording. Continuous spectral analysis was performed on the electroencephalogram (EEG) to obtain theta power (6–9 Hz) and delta power (0–4 Hz), as well as the R-R interval signals in order to quantify the high-frequency power (HF) and normalized low-frequency power (LF%) that are used to assess parasympathetic and sympathetic activity, respectively. All animals underwent a sleep deprivation experiment and a control experiment (6-h intervention and 1-h recovery period) on two separate days. During sleep deprivation, HF and theta power during wakefulness were significantly higher than during the control wakefulness after the second hour and first hour, respectively. During recovery non-rapid eye movement sleep, there was a rebound in sleep time and delta power as well as an elevation in HF relative to control post-intervention sleep. Both the rise in HF and theta power during extended wakefulness were found to be positively correlated with the delta power rebound. Furthermore, the HF change during extended wakefulness was also correlated with the amount of sleep loss and the enhancement of waking theta power. Our finding suggests that waking parasympathetic activity intimately reflects the cumulative sleep pressure, suggesting a potential role to be an autonomic marker for sleep propensity.

Long-lasting enhancement of rapid eye movement sleep and pontogeniculooccipital waves by vasoactive intestinal peptide microinjection into the amygdala temporal lobe.

The effect of a vasoactive intestinal peptide (VIP) microinjection into the amygdaloid central (CN) and basal nuclei (BN) on sleep organization and on the number and pattern of occurrence of pontogeniculooccipital (PGO) waves was analyzed. One group of 8 cats was studied in baseline conditions and after the microinjection of two doses of VIP applied into the CN and BN. Sleep research laboratory. PARTCIPANTS AND INTERVENTIONS: Eight cats were prepared with sleep-recording electrodes and with guide tubes in both amygdalae for saline and VIP microinjections. Neuropeptide doses of 0.10 microg/1 microl (30 microM) and 0.33 microg/1 microl (99.24 microM) were employed. Once the microinjection was applied, 23-hour polygraphic sleep recordings were performed for 5 consecutive days. Concomitantly the PGO waves were tape-recorded on each day and computationally analyzed. Results show that the 0.10 microg/1 microl microinjection produced no change. Unilateral VIP 0.33 microg/1 microl injection into the CN provoked a significant and lasting increase in the percentage of slow-wave sleep with PGO waves. Bilateral application of VIP increased the percentage of slow-wave sleep with PGO waves and rapid eye movement sleep for 5 days. Bilateral microinjection of the neuropeptide into the BN only enhanced the percentage of slow wave sleep with PGO waves. For both amygdaloid nuclei, we observed that VIP increased the number and modified the PGO wave pattern of occurrence during slow-wave sleep with PGO waves and during rapid eye movement sleep. The VIP microinjection into both the CN and BN induces increased amounts of rapid eye movement sleep, PGO waves, and slow-wave sleep with PGO waves, having a more robust effect on all of these three variables when applied into the CN.

Copulatory activity increases slow-wave sleep in the male rat.

It is believed that sexual activity increases the need to sleep in many species. However, the relationship between copulatory activity and sleep has been poorly studied. Several studies have observed variations in the sleep of female rats and women as a function of their reproductive state. These effects have been correlated with the effects of female steroid hormones, but not with sexual activity. The aim of the present study was to evaluate the sleep-wake pattern of male rats immediately after different conditions of copulatory activity. Sexually experienced male rats were chronically implanted with a standard set of electrodes for sleep recording. After a control sleep recording of 8 h, the males were randomly assigned to one of the following experimental conditions: 30 min in the presence of an ovariectomized (OVX) rat; 30 min in the presence of an intact non-receptive female (NRF); with a receptive female until reaching one ejaculation (1E); and with a receptive female until reaching three ejaculations (3E). In addition, after 10 days, males were randomly exposed to one of the following copulatory conditions during 4 h: to remain in the presence of an OVX rat; to remain in the presence of an NRF female, and with receptive females until reaching sexual satiety (SS). Male sexual behavior was assessed just after the onset of the dark period, and sleep recordings were obtained during 8 h immediately after experimental testing. Both the three ejaculations group (3E) in the first experiment and the sexual satiety group (SS) in the second experiment showed enhanced percentages of time spent in slow wave sleep (SWS) II and a shorter latency to the first SWS II episode than in the control group or under basal conditions. In addition, neither the presence of a non-receptive female or an OVX female, nor sexual behavior until reaching one ejaculation induced any effect on the sleep stages. These findings suggest that the increase in SWS II induced by both 3E and SS may be governed by some specific mechanism that is essentially independent of physical exercise or stress. Copulatory activity might be the source of neurohormonal processes that induce sleep and may involve the participation of gamma-aminobutyric acid, serotonin or other endogenous regulators of sleep and wakefulness. Nevertheless, the precise mechanism by which the sexual behavior increases SWS is still to be determined.

How accurately does wrist actigraphy identify the states of sleep and wakefulness?

Because sleep and wakefulness differ from each other by the amount of body movement, it has been claimed that the two states can be accurately distinguished by wrist actigraphy. Our objective was to test this claim in lengthy polysomnographic (psg) and actigraphic (acf) samples that included night and day components. Fourteen healthy young (21-35 years) and old (70-72 years) men and women lived in a laboratory without temporal cues for 7 days. Each subject continuously wore sleep-recording electrodes as well as 2 wrist-movement recorders. Act measurements were converted to predictions of sleep and wakefulness by simple-threshold and multiple-regression methods. Psg served as the gold standard for calculation of predictive values (PV, the probability that an act prediction is correct by psg criteria). N/A. N/A. N/A. The 7-day act recordings showed clear circadian cycles of high and low activity that respectively corresponded to subjective days, when subjects were wakeful, and subjective nights when they slept. Lower act levels corresponded to deeper states of psg sleep. Logistic regression on a 20-minute moving average of act gave the highest overall PV's. Nevertheless, the mean PV for sleep (PVS) was only 62.2% in complete, day + night samples. PVS was 86.6% in night samples. Act successfully predicted wakefulness during subjective nights (PVW = 89.6) and accurately measured circadian period length and the extent of sleep-wake consolidation, but it overestimated sleep rate and sleep efficiency. Act systematically decreased before sleep onset and increased before awakening, but reliable transitions among joint psg/act states (the Markov-1 property) were not demonstrated. Low PV's and overestimation of sleep currently disqualify actigraphy as an accurate sleep-wake indicator. Actigraphy may, however, by useful for measuring circadian period and sleep-wake consolidation and has face validity as a measure of rest/activity.

Effects of amygdala lesions on sleep in rhesus monkeys

The amygdala is important in processing emotion and in the acquisition and expression of fear and anxiety. It also appears to be involved in the regulation of sleep and wakefulness. The purpose of this study was to assess the effects of, fiber-sparing lesions of the amygdala on sleep in rhesus monkeys ( Macaca mulatta). We recorded sleep from 18 age-matched male rhesus monkeys, 11 of which had previously received ibotenic acid lesions of the amygdala and seven of which were normal controls. Surface electrodes for sleep recording were attached and the subjects were seated in a restraint chair (to which they had been adapted) for the nocturnal sleep period. Despite adaptation, control animals had sleep patterns characterized by frequent arousals. Sleep was least disrupted in animals with large bilateral lesions of the amygdala. They had more sleep and a higher proportion of rapid-eye-movement (REM) sleep than did either animals with smaller lesions or control animals. Based on these results, it seems likely that, in the primate, the amygdala plays a role in sleep regulation and may be important in mediating the effects of emotions/stress on sleep. These findings may also be relevant to understanding sleep disturbances associated with psychopathology.

Changes in sleep after acute and repeated administration of nicotine in the rat.

Acetylcholine clearly plays a role in regulating sleep. This influence may involve nicotinic systems because several studies have demonstrated that nicotine treatment alters sleep. However, the literature that suggests an effect of nicotine treatment on sleep is contradictory, perhaps because different doses and routes of administration were used. The studies reported here evaluated the effects of several doses of nicotine on REM sleep in the rat. Male Wistar rats were prepared with a set of sleep recording electrodes and, following habituation to the test chamber, were used in one of three studies: a) a dose-response analysis of an acute dose of nicotine on REM sleep measured during the first 4 h after injection; b) a chronic treatment experiment; or c) a mecamylamine blockade experiment. Acute nicotine administration decreased REM sleep in a dose-dependent fashion; significant effects were observed following injection with the 0.5 and 1.0 mg/kg doses. A decrease in slow wave sleep and an increase in wakefulness were also observed. Mecamylamine by itself did not affect REM sleep, but it blocked the effects on sleep produced by nicotine when given 30 min before a 1 mg/kg dose of nicotine. Rats that had been injected once daily with a 0.1 mg/kg dose of nicotine showed an increase in REM sleep after the third injection, whereas rats that had been chronically treated with a higher dose (0.5 mg/kg) displayed a reduction in REM and total sleep time. These findings argue that the effects of both acute and chronic nicotine treatment on sleep are influenced by the dose of nicotine used.

Acetylcholine releases of mesopontine pgo-on cells in the lateral geniculate nucleus in sleep-waking cycle and serotonergic regulation

1. 1. Five adult cats were prepared with standard sleep-recording electrodes, microinjection cannulae in the bilateral mesopontine tegmentum X area and cannulae for microdialysis probes in the LGN. 2. 2. Dialysates were collected at 5 min intervals during SWS, REM sleep and wakefulness, and during pre- and post-stimulation periods of 5MeODMT microinjection in the bilateral mesopontine tegmentum of freely moving cats. 3. 3. A REM sleep-specific increase of ACh release was observed in the LGN, but not out of the LGN. 4. 4. ACh release was depressed up to 33% by bilateral SMeODMT microinjection in the mesopontine tegmentum where the microinjection of carbachol also depressed ACh in the LGN probably by stimulating the auto receptor. 5. 5. Our observations indicate that PGO-on neurons of mesopontine tegmentum release more ACh in the LGN during REM sleep by burst discharge than during wakefulness and SWS, and that presumptive cholinergic PGO-on cells are regulated by serotonergic inputs.

Cholinergic antagonists and REM sleep generation

In this study we extended our observations on the role of M 1 and M 2 muscarinic receptors in mediating the cholinergic induction of REM sleep. Cats were chronically implanted with sleep recording electrodes and microinjections of Ringer's or muscarinic antagonists followed by the relatively specific M 2 muscarinic agonist, cis-methyl-dioxolane (cisdioxo), were made into the medial pontine reticular formation (mPRF). The microinjection of Ringer's followed by cisdioxo significantly increased REM sleep percentage. Atropine, a mixed muscarinic receptor antagonist, administered before cisdioxo blocked the REM sleep increase while pirenzepine, a selective M 1 muscarinic antagonist, did not block the cisdioxo-induced increase in REM sleep. Gallamine, a nicotinic and a putative M 2 antagonist, tended to inhibit the cisdioxo-induced increase in REM sleep. These results support the hypothesis that the cholinergic stimulation-induced REM sleep in the medial pontine reticular formation is mediated by a non-M 1 muscarinic receptor subtype.

Relation of pontine choline acetyltransferase immunoreactive neurons with cells which increase discharge during REM sleep

The purpose of this study was to determine whether neurons in the medial pontine reticular formation with high discharge rates during REM sleep could be localized in regions of the brainstem having neurons displaying choline acetyltransferase immunoreactivity. Six cats were implanted with sleep recording electrodes and microwires to record extracellular potentials of neurons in the pontine reticular formation. Single-units with a S:N ratio greater than 2:1 were recorded for at least two REM sleep cycles. A total of 49 units was recorded from the pontine reticular formation at medial-lateral planes ranging from 0.8 to 3.7 mm. The greatest proportion of the units (28.6%) showed highest discharge during active waking and phasic REM sleep compared to quiet waking, non-REM sleep, transition into REM sleep or quiet REM sleep periods. A percentage (20.4%) of the cells had high discharge associated with phasic REM sleep periods while 8.2% of the cells showed a progressive increase in discharge from waking to REM sleep. Subsequent examination of the distribution of choline acetyltransferase immunoreactive cells in the PRF revealed that cells showing high discharge during REM sleep were not localized near presumed cholinergic neurons. Indeed, we did not find any ChAT immunoreactive somata in the medial PRF, an area which has traditionally been implicated in the generation of REM sleep. These results suggest that while increased discharge of PRF cells may be instrumental to REM sleep generation, these cells are not cholinergic.

Diurnal rhythm of plasma immunoreactive beta-endorphin and its relationship to sleep stages and plasma rhythms of cortisol and prolactin.

To determine the diurnal rhythm of plasma beta-endorphin (beta-End), 10 healthy male volunteers between the ages of 20 and 32 yr were studied in a sleep laboratory setting for a 24-h period. Blood samples were taken through an indwelling catheter at 0800, 1000, 1400, 1800, 2200, 2300, and 2400 h and then half-hourly until 0730 h, and they were then assayed for total beta-End-like immunoreactivity (ir beta-End), PRL, and cortisol. Subjects were habituated by spending the night before the study in the sleep laboratory with an indwelling catheter and electrodes for sleep recording in place. There was a clear diurnal variation of ir beta-End, with lowest levels between 2200 and 0330 h and highest levels between 0400 and 1000 h. There was no evidence for direct entrainment with sleep stage. There was a close correlation with cortisol levels, suggesting a similar secretory pattern for beta-End and PRL in only 5 of the subjects. Because the beta-End antiserum used has a cross-reactivity of 30% with beta-lipotropin gel permeation chromatography was done on extracts of plasma taken at 1400, 2400, 0400, and 0730 h for each subject. The peak in the beta-End elution position showed a clear diurnal variation similar to that of ir beta-End.