Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to determine whether ponto-geniculo-occipital (PGO) spikes play a role in triggering or maintaining sleep. During the recording of the sleep cycle of cats, the appearance of the first PGO spike automatically triggered an auditory stimulus through a speaker placed in the cat's recording cage. The effect of this procedure was compared to similar period when no such stimulus was given. The results showed that the auditory stimulus increased PGO spike density during REM sleep. It also produced a spectacular increase in the duration of REM, while decreasing the latency of its appearance from the first PGO spike. It is suggested that the auditory stimulus reinforces the 'PGO system', which in turn may function as a pace-setter for priming and maintaining REM sleep.
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PMID:Increasing PGO spike density by auditory stimulation increases the duration and decreases the latency of rapid eye movement (REM) sleep. 664 Mar 22

The confounding effects of undernourishment and body cooling, resulting from maternal separation, were investigated by separating food and warmth deprivation. Rat pups aged 3-16 d were deprived of food for alternate 24-h periods by removal from the lactating mother. Some of the pups were placed with a foster mother, who kept them warm, whereas others were put in an empty cage at 22 degrees which resulted in a sharp drop in body temperature. Pups which were kept warm showed great fluctuations in weight between periods of starvation and feeding. The cooled pups lost less weight during deprivation but also recovered less on refeeding. The resultant growth rate was much lower in non-fostered (i.e. cooled) than in fostered pups. Up to the age of 8 d, cooled pups failed to raise their body temperature above that of the surroundings and did not digest the milk in their stomachs. Although, thereafter, they were able to raise their temperature to 26 degrees and to digest stomach contents, the extra energy expended resulted in more severe growth restriction. One-third of the pups died at 16 d but the rest were quickly rehabilitated by ad lib. feeding and showed a normal growth rate, although they remained smaller than the controls. The development of nipples, hair, eye opening and vaginal opening was related more to chronological age than to weight. A side effect of cooling was an almost complete abolition of active (REM) sleep, which is normally very high in infants; a slight rebound increase in active sleep was seen at 21 d. Direct as well as side effects of cooling may thus be responsible for some of the observed consequences of maternal separation.
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PMID:Effects of cooling in infant rats on growth, maturation, sleep patterns and responses to food deprivation. 674 34

To determine whether the recently increased sensitivity of the variable frequency oscillator and the use of separate rib cage and abdominal transducers made calibration of the Respitrace system easier, we performed 106 different calibration procedures against a pneumotachygraph in 36 normal infants, 41 using 2 separate periods of quiet sleep, 49 using quiet and REM sleep, and 16 using 2 separate periods of REM sleep. When the calibration was done using 2 separate periods of quiet sleep, or using periods of quiet and REM sleep, a change of at least 50% in the amplitudes of both the abdominal and rib cage signals between the 2 sleep periods, gave accurate calibration factors in 92%, compared with only 30% when the amplitude of either signal changed by less than 50%. Calculation of the calibration factors can be done either by the least squares method or by solving simultaneous equations with no significant difference between the results.
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PMID:Calibration of respiratory induction plethysmography (Respitrace) in infants. 712 47

The hyperresponsiveness to apomorphine disappears after REM sleep deprivation of rats; the time course of the disappearance was investigated. When REM sleep-deprived (REMd) rats were caged individually during the recovery period the increase in ambulation and in stereotyped behaviour elicited by apomorphine subsided within 8-24 h; on the other hand, the exaggerated aggressiveness persisted up to 64 days. However, when the deprived rats were allowed to recovery in groups of 3 per cage the increase in aggressiveness subsided after 4 days. Since individual housing of non-deprived rats for 4--11 days increased the apomorphine-aggressiveness steadily, 'isolation' probably summed with REM deprivation in facilitating the effects of apomorphine on aggressive behaviour. The results also suggest that the dopaminergic systems implicated in aggressive behaviour are sensitized by REM deprivation for a longer period than those subjacent to ambulation and stereotype.
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PMID:The persistence of hyperresponsiveness to apomorphine in rats following REM sleep deprivation and the influence of housing conditions. 720 5

REM sleep deprivation (RSD) of rats results in facilitation of dopaminergic behavior and an increase in striatal D2 receptor density. To determine whether RSD results in changes in D2 receptor in other brain regions, receptor affinity (Kd) and density (Bmax) were measured in the anteromediofrontal (AM), cingulate (CN), and sulcal cortex (SL) in four groups of rats: 1), RSD96 group (RSD for 96 h; small pedestal/water tank method), 2) RSD24 group (large pedestals for 72 h then small pedestals for 24 h), 3) tank control group (TC; large pedestals for 96 h), and 4) cage control group. In separate groups, ambulation was recorded for 30 min following treatments. Group RSD96 showed an increase in activity compared to TC, and TC was increased compared to CC (p < 0.05 for all). In group RSD24, the AM showed an increase in Bmax and Kd (p < 0.05), but there were no effects by RSD96. In the CN, Bmax and Kd were decreased by RSD96 (p < 0.05) but not RSD24. In the SL, Bmax was increased by RSD96, but not RSD24, whereas Kd was increased in both RSD groups (p < 0.05).
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PMID:REM sleep deprivation alters dopamine D2 receptor binding in the rat frontal cortex. 750 77

Patients with cystic fibrosis (CF) often hypoventilate during sleep with marked falls in oxygen saturation (SaO2%). This occurs most commonly during REM sleep, when there is a reduction in rib cage excursion and a fall in end-expiratory lung volume (EELV). The aim of this study was to examine the effect of nocturnal nasal continuous positive airway pressure (nCPAP) on SaO2 and the respiratory disturbance index (RDI) during sleep in patients with CF and severe lung disease. Seven patients (FEV1% pred, 23 +/- 5; range, 14 to 28%) were evaluated during sleep on two nights, control and nCPAP (11 +/- 2 cm H2O; range, 8 to 16 cm H2O), with four patients breathing room air and three patients breathing supplemental oxygen on both nights. Mean awake SaO2 was 91 +/- 1% (range, 89 to 93%). All patients showed significant oxyhemoglobin desaturation and respiratory disturbance in the control study. The maximal falls in SaO2 (15 +/- 10%) were most often associated with phasic eye movements, and a decline in rib cage excursion and the sum signal (Respitrace) during REM sleep. Nasal CPAP resulted in a significant improvement in the mean minimum oxygen saturation (MMOS) during both NREM (nCPAP 91 +/- 3% vs control 88 +/- 2%, p < 0.05) and REM sleep (nCPAP 89 +/- 6% vs control 83 +/- 6%, p < 0.05). Transcutaneous CO2 measurements were not significantly different between the control and the nCPAP studies. The RDI was also significantly reduced with nCPAP especially during REM sleep (9 +/- 7 events per hour vs control 25 +/- 11 events per hour, p < 0.05). Nasal CPAP caused no change in total sleep time or sleep efficiency yet significantly reduced the RDI and improved baseline SaO2 during both NREM and REM sleep.
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PMID:Benefits of nocturnal nasal CPAP in patients with cystic fibrosis. 798 90

Rats subjected to chronic total sleep deprivation (TSD) by the disk-over-water method have shown very large, sustained rebounds in paradoxical sleep (PS) (also known as REM sleep). Other studies have indicated that cholinergic mechanisms are involved in the instigation and maintenance of PS. Hypothetically, the large PS rebounds could be mediated by an upregulation of cholinergic receptors during TSD. To evaluate this hypothesis, regional brain cholinergic receptors were compared in rats subjected to 10-day TSD by the disk-over-water method (TSD rats), yoked control (TSC) rats which received the same physical stimulation but with much smaller reductions in sleep, and home cage control (HCC) rats. L-[3H]nicotine and [3H]quinuclidinyl benzilate were used as specific cholinergic radioligands for nicotinic and muscarinic receptor binding assays, respectively. Nicotinic receptor binding was not significantly different among groups for any of the brain regions assayed, including frontal cortex, parietal cortex, thalamus, amygdala, hippocampus, anterior hypothalamus, posterior hypothalamus, caudate, limbic system (including septal area, olfactory tubercle, and nucleus accumbens), midbrain, pons, and medulla. Thus, there was no evidence that changes in nicotinic receptors mediate the PS rebounds. For muscarinic receptor binding, TSD rats differed significantly from control rats only in showing a higher binding affinity than TSC rats in the limbic system and a lower binding density than HCC rats in the hippocampus. On the other hand, significant differences in muscarinic receptor binding sites between rats selectively deprived of PS and their yoked controls were found only for the septal area.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of chronic sleep deprivation on central cholinergic receptors in rat brain. 803 5

Rats were deprived of REM sleep (REMS) for 72 h with the platform method and decapitated in the morning immediately after the deprivation or in the afternoon after having been allowed 5 hours of rebound sleep. The histamine concentrations of the anterior and posterior hypothalamus, the cortex, the hippocampus and the pineal gland were measured, as well as the tele-methylhistamine concentrations of the anterior and posterior hypothalamus. Histamine concentrations were no different after REMS deprivation compared to large platform or dry cage controls, but in the anterior hypothalamus histamine levels increased during rebound sleep only in the REMS deprived rats. tele-Methylhistamine/histamine ratios were higher after 72 h of both REMS deprivation and the large platform treatment compared to dry cage controls, indicating increased histamine utilization during the platform treatment procedure.
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PMID:The effect of REM sleep deprivation on histamine concentrations in different brain areas. 817 13

The aim of this study was to assess whether age-related changes in thoracic shape modify patterns of thoracoabdominal asynchrony (TAA) or applicability of phase angle analysis during sleep in young children with increased respiratory loads. We assessed TAA during polysomnographic monitoring in 14 young children (mean age 32 months, range 19 to 46; mean weight 12.5 kg, range 9.3 to 17) with severe bronchopulmonary dysplasia (BPD). Of the patients 10 were severely enough affected to require tracheostomy. We measured asynchrony of rib cage (RC) and abdominal (AB) movements at midinspiration and the corresponding phase angle from oscillographic recordings during both non-REM and REM sleep. We measured the amplitude of "paradoxical" displacement of either RC or AB during inspiration and expressed this as a percentage of the total displacement of the compartment. Of 9 children who manifested early inspiratory AB paradox during non-REM sleep, 7 showed a figure eight on the Konno-Mead diagram. The magnitude of abdominal paradox during non-REM sleep was significantly positively correlated with age (n = 14, r = 0.68; p < 0.01). Phase angle was significantly negatively correlated with dynamic lung compliance (n = 14, r = -0.66; p < 0.01). During REM sleep, expiratory abdominal muscle activity was abolished and all patients with abdominal paradox "converted" to an open loop with RC paradox during inspiration. Graphic assessment of the Lissajous figure on the Konno-Mead diagram indicated when midinspiratory phase angle analysis did not reflect the severity of TAA and can be used to infer patterns of respiratory muscle recruitment. We conclude that young children manifest patterns of TAA that differ from the early inspiratory RC paradox commonly observed in infants. Comparison of RC-AB loops between non-REM and REM sleep in the same child can assess increased thoracic inspiratory efforts and expiratory muscle activity as potential mechanisms for abdominal paradox, as distinct from diaphragm ineffectiveness.
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PMID:Asynchronous chest wall movements during non-rapid eye movement and rapid eye movement sleep in children with bronchopulmonary dysplasia. 848 28

The GABAB antagonist CGP 35348 was intraperitoneally given in doses of 100, 300, and 900 mg/kg to old rats. These rats were earlier chronically provided with EEG and EMG electrodes. Sleep recordings based on visual inspection of EEG and EMG recordings were made for 3 h post injection, and spontaneous behaviour in the recording cage was additionally observed. With 100 and 300 mg/kg, the drug produced an increase in the duration of REM sleep compared to the saline-injected control group. The REM sleep latency was correspondingly reduced. Non-REM sleep and total sleep duration increased and an s-shaped dose-response relationship was found. Explorative behaviour was diminished after injections with 100 and 300 mg/kg CGP 35348. The number and duration of spike-wave discharges were reduced after all doses of CGP 35348 and during all 3 recording hours. The latter outcomes confirm the strong suppressive action of this drug on spike-wave discharges; these effects have also been reported in models of absence epilepsy. The hypnotic properties and especially the increase in REM sleep after the administration of CGP 35348 deserve attention considering the paucity of drugs which facilitate REM sleep. The discovery of drugs promoting REM sleep might have theoretical as well as clinical consequences.
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PMID:Effects of the GABAB antagonist CGP 35348 on sleep-wake states, behaviour, and spike-wave discharges in old rats. 873 75


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