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Biomedical subjects

W B Mendelson

Publications and source records attributed to W B Mendelson.

157 records · Page 9Linked to original sources
PubMed1975

Suppression of sleep-related prolactin secretion and enhancement of sleep-related growth hormone secretion.

Methysergide, a clinically-used blocker of serotonin receptors, was administered to 10 normal young men at a dose of 2 mg every 6 h for 48 h. After drug treatment, serum levels of growth hormone during sleep were 41.9% higher than placebo values (less than 0.001). In contrast, drug treatment was associated with a 36.4% decrease in stimulated growth hormone secretion during insulin tolerance testing (P less than 0.01). These opposite effects of methysergide suggest that different mechanisms are responsible for sleep-related and insulin-induced growth hormone secretion. Accordingly, data obtained with pharmacologic stimuli may lead to erroneous inferences regarding physiologic growth hormone control mechanisms. Administration of methysergide profoundly suppressed sleep-related prolactin secretion; overall nocturnal mean prolactin fell by 70.3% from 4.30+/-0.19 to 1.28+/-0.06 ng/ml (P less than 0.0001). It appears that serotonin may be significant modulating neurotransmitter for the control of growth hormone secretion, limiting sleep-related release, and enhancing insulin-induced release. It seems likely from these data that the role of serotonin in the control of prolactin secretion is relatively more important, since serotonin receptor blockade dramatically reduced sleep-related prolactin secretion.

Adult↗
PubMed1975

Serotonin inhibition and sleep.

Methysergide a clinically used blocker of serotonin receptors, was given for 48 hr to 11 normal adults, at a dose of 8 mg per 24 hr. Total REM sleep time was decreased, although total sleep time was unchanged. Stage 4 decreased and stage 3 increased, while total slow wave sleep remained constant. There was a tendency toward a decrease in the number of intact sleep cycles. The relationship of these data to published reports on p-chlorophenylalanine is discussed.

Administration, Oral↗
PubMedDate not supplied

The role of central and peripheral cholecystokinin in mediating appetitive behaviors.

Cholecystokinin (CCK) reduces total food consumption in mice, rats, pigs, sheep, monkeys and humans. Behaviors associated with an underlying state of satiety are reported after CCK administration. Reductions in exploration and social interactions by CCK are not due to true sedation or sleep, as measured by cortical EEG recordings. The satiety effects appear to be mediated by peripheral CCK receptors, through a feedback loop involving the vagus nerve. The conceptual link between the behavioral functions of CCK as a putative satiety signal and its established digestive functions are discussed.

Animals↗
PubMedDate not supplied

Picrotoxinin receptor ligand blocks anti-punishment effects of alcohol.

Ethanol at low doses produces a release of punished responding in an operant rat conflict test similar to that observed for benzodiazepines and phenobarbital. It has been hypothesized that these anti-punishment effects are mediated via the GABA-benzodiazepine receptor-ionophore complex but not at the benzodiazepine binding site. In the present study isopropylbicyclophosphate (IPPO), which binds at the picrotoxinin site, reversed the release of punished responding produced by ethanol, pentobarbital and chlordiazepoxide; at low doses IPPO (less than 10 micrograms/kg) appeared to be most effective against ethanol but at higher doses (greater than 15 micrograms/kg) was also effective against pentobarbital and chlordiazepoxide. At still higher doses IPPO produced a decrease in punished and unpunished responding. These results suggest that the "anxiolytic" actions of ethanol may involve a direct action on the GABA-benzodiazepine receptor-ionophore complex and this action may underlie some of the intoxicating effects of ethanol.

Animals↗
PubMedDate not supplied

Age-dependent changes in recovery sleep after 48 hours of sleep deprivation in rats.

To characterize possible changes in homeostatic regulation of sleep with aging, we have examined sleep stages during recovery sleep after 48 h of sleep deprivation in young (3 months), middle aged (12 months), and old (24 months) rats. It was found that young and middle aged, in contrast to old rats, had large (21-24%) increases in total sleep time during recovery sleep; the old rats experienced a quantitatively small (8%) but significant rise in total sleep. NREM sleep increased significantly during the recovery period in young and middle aged, but not older rats. High voltage NREM sleep (HS2) declined by 30% during recovery in the young animals, but remained unchanged compared to baseline in the middle aged and old animals. The young and middle aged rats had increases in REM sleep during recovery compared to their baseline by 96% and 93%, respectively, which was significantly greater than a 65% increase during recovery in the old rats. Increases in total sleep and REM sleep during recovery were largely confined to the first 6 h in young and middle aged rats, but maxima for the old rats occurred in the second 6 h.

Aging↗
PubMedDate not supplied

EEG delta power during sleep in young and old rats.

Delta EEG power density, which has been viewed as a measure of intensity of NREM sleep, declines across the lifetime in humans, cats, and hamsters, but data in rats have been unclear. It is also uncertain whether older rats differ from younger animals in the degree of change in delta power during recovery sleep following short-term sleep deprivation. We have examined delta power density in NREM sleep under baseline conditions and following 48 h of sleep deprivation in young (3 months), middle-aged (12 months), and older (24 months) rats. The presence or absence of age effects was highly dependent on the method of normalizing the data. When expressed as a fraction of total NREM EEG power, there was no age effect on baseline delta power density, or on the change from baseline to recovery conditions. When expressed as a multiple of delta power in REM under the same condition, the younger rats had higher delta power density than the middle-aged and older rats. For all the ages combined, there was an increase in delta power density in the recovery condition. When examined by age, the younger rats (which started from a higher level of delta power density than the other groups) did not have an increase in delta during recovery; the middle-aged rats tended to, and the older rats (which started from lower baseline levels) significantly increased delta power density in the recovery condition. This suggests that the lower delta power seen during baseline in older rats is not due to decreased ability to generate delta activity.

Aging↗
PubMedDate not supplied

Use of the sleep laboratory in suspected sleep apnea syndrome: is one night enough?

BACKGROUND: Sleep-disordered breathing appears to vary widely from night to night in the general population. OBJECTIVE: To determine the difference in accuracy of diagnosing sleep apnea when there are one vs two sleep recordings in a clinical population. METHODS: Fifty patients clinically suspected of having obstructive sleep apnea underwent polysomnography for two nights. RESULTS: The number of episodes of apnea or hypopnea per hour (the apnea-hypopnea index, AHI) on each night was highly correlated (r = .86), and there were no significant differences between the two nights in duration of episodes, mean minimal arterial oxygen desaturation, or absolute minimum desaturation. On the first night, 46 patients had an AHI of 5 or more; on the second night 49 did. Similarly, 42 patients had an AHI of 10 or more on the first night; on the second night 46 did. All patients with an AHI of 5 or more on the first night also had an AHI of 5 or more the second night, and only one patient who had an AHI of 10 or more on the first night did not on the second night. In contrast, some nonrespiratory variables improved on the second night. CONCLUSIONS: One night of testing should generally suffice. A second recording might be expected to be positive in half of the small group of patients clinically suspected of having sleep apnea who have a negative first study.

Clinical Laboratory Techniques↗
PubMedDate not supplied

A signal analysis approach to rat sleep scoring instrumentation.

Automated rat sleep analysis focuses on the statistically regular waveforms of the EEG, such as theta and delta rhythms. Such stochastic processes can be quantified in several manners. Time domain statistics such as auto- and cross-correlations produce outputs that are difficult to use and are best performed in software. Frequency domain statistics like spectral density accurately quantify the sleep state by power-frequency distributions but also require sophisticated computer processing. Continuous frequency analysis, using pass-band filtering, accurately measures signal power in an on-line fashion and employs relatively inexpensive hardware to estimate power by integrating the square of the signal. This method differs substantively from other previously reported systems which rely on signal amplitude analysis. Comparison of this system with a human scorer indicates high degrees of validity and reproducibility.

Animals↗