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Biomedical subjects

I Feinberg

Publications and source records attributed to I Feinberg.

At least 37 records · Page 2Linked to original sources
PubMed1996

NREM delta stimulation following MK-801 is a response of sleep systems.

1. We have previously shown that noncompetitive blockade of the N-methyl-D-aspartate (NMDA)-gated cation channel with ketamine or Dizocilpine maleate (MK-801) increases the intensity of non-rapid-eye-movement (NREM) delta during subsequent sleep. This delta increase [measured as integrated amplitude (IA) in 1- to 4-Hz electroencephalogram (EEG)] occurs in the 12-h period following intraperitoneal injection. However, the 12 h after drug injection is also the period in which these drugs induce neurotoxic changes, raising the possibility that the increased delta represents toxic EEG slowing rather than an increase in the physiological delta waves of NREM sleep. 2. We hypothesized that the time course of delta stimulation could be separated from the time course of neurotoxicity. We tested this hypothesis by injecting 0.3 mg/kg MK-801 at the start of the dark period (DP) and depriving rats of sleep until the onset of the light period (LP) 12 h later. 3. There were two control groups: one received MK-801 at the start of the DP with no further manipulation, and the second received a saline injection at DP onset followed by 12 h of sleep deprivation. The dependent variable was the amount of delta IA in the LP, whose onset was 12 h after MK-801 injection. Total IA in the LP was significantly greater in rats that received MK-801 followed by sleep deprivation than in rats that received sleep deprivation alone or MK-801 alone. 4. This finding indicates that delta stimulation by MK-801 is maintained over 12 h of waking, indicating that the delta increase is not due to toxic EEG slowing or persisting MK-801. Instead, NMDA channel blockade by MK-801 increases the homeostatic need for delta or else directly alters sleep regulatory systems. We speculate that these effects are mediated by hypothalamic sleep centers through control of neuroendocrine pulses that produce both NREM and rapid-eye-movement sleep. 5. Imposing a period of waking between drug administration and sleep onset may prove a generally useful strategy for determining whether a drug affects the homeostatic need for sleep or acutely stimulates sleep systems. This strategy can also help distinguish between toxic and physiological increases in delta EEG.

Animals↗
PubMed1996

Noncompetitive NMDA channel blockade during waking intensely stimulates NREM delta.

We previously found that subanesthetic doses of ketamine administered during the dark (active) period (DP) in rats strongly increased the integrated amplitude of the delta (1-4 Hz) electroencephalogram (EEG) in subsequent nonrapid eye movement (NREM) sleep. Here, we injected MK-801 into adult male Sprague-Dawley rats to test the hypothesis that such delta stimulation is characteristic of drugs that noncompetitively block the cation channel gated by the N-methyl-D-aspartate (NMDA) receptor. Injections of 0.3 and 0.5 mg/kg MK-801 in the middle of the DP produced waking intoxication for approximately 3 hr. In the following light period, NREM delta integrated amplitude was markedly increased in every rat (mean 55% increase after 0.5 mg/kg). A separate control experiment with 3-hr sleep deprivation in the mid-DP showed that the delta stimulation could not be attributed to sleep loss during MK-801 intoxication. Mechanisms by which NMDA cation channel blockade might stimulate NREM delta include a compensatory (homeostatic) sleep response to the metabolic, receptor or other neuronal effects of cation channel blockade; pathologic EEG slowing caused by neurotoxicity (in which case NREM delta might provide a noninvasive index of neurotoxic vacuolization); or a persistent, direct action of the drug or its metabolites on delta-generating systems. Questions of mechanism gain interest because of the magnitude of these pharmacologic effects on the sleep EEG component (delta) thought to be correlated with brain recuperative processes. In addition, our findings add to growing evidence implicating excitatory amino acid systems in sleep regulation.

Animals↗
PubMed1995

Intraperitoneal dizocilpine induces cortical spike-wave seizure discharges in rats.

Dizocilpine has been shown to be anticonvulsant in several experimental models of epilepsy. Nevertheless, 0.3 or 0.5 mg/kg intraperitoneal (i.p.) dizocilpine produced cortical spike-wave discharges (SWDs) in four of seven rats. The SWDs were accompanied by behavioral arrest, and also showed: a narrow range of induction times (around 25 min post-injection); hippocampal spikes closely correlated with the cortical spikes of the SWDs; a precipitous drop out of fast (45-100 Hz) cortical EEG; myoclonic bursts in nuchal EMG that began during the cortical slow waves. These findings suggest that patients being treated experimentally for stroke with non-competitive N-methyl-D-aspartate (NMDA) cation channel blockers should be monitored for seizures.

Animals↗
PubMed1994

Sigma (12-16 Hz) and beta (20-28 Hz) EEG discriminate NREM and REM sleep.

All night sleep EEG from ten normal students were subjected to FFT spectral analyses. Delta (0.3-3 Hz), sigma (12-16 Hz) and beta (20-28 Hz) EEG showed strongly oscillating patterns across the night. The scattergram of sigma versus beta revealed two separate clusters. One cluster demonstrated a positive linear correlation between sigma and beta. The second cluster showed a range of beta, but a stable, low level of sigma activity. Points in the former cluster consisted of those from NREM epochs, and in the latter, from REM epochs. The present results suggest that REM and NREM EEG are composed of two sets of EEG frequency components, perhaps reflecting different neuronal pools.

Adult↗
PubMed1994

Dream report length is more dependent on arousal level than prior REM duration.

Twenty two young adult subjects (Ss) were monitored for 2 consecutive nights in the sleep laboratory. Each S was awakened three times per night: at sleep onset and during the second (REMP2) and fourth (REMP4) REM periods. Length of time in each REMP prior to awakening was either 5 or 10 min, counterbalanced on successive nights. Sleep mentation reports were obtained by standardized interview and scored for total word count (TWC). TWC after 5 min of prior REM sleep did not differ significantly from TWC after 10 min of prior REM sleep. However, mean TWC from REMP4 awakenings was almost twice that from REMP2 awakenings. These findings are consistent with the hypothesis that the amount of recall from experimental REM awakenings depends on central arousal level and its effects on mnemonic processes.

Adult↗
PubMed1993

Dissociation of delta EEG amplitude and incidence in rat NREM sleep.

The delta (1-4 Hz) EEG of nonREM (NREM) sleep was subjected to period/amplitude analysis in 10 Sprague-Dawley rats. During NREM sleep in the 12-h light period, average delta wave amplitude and delta wave incidence (halfwaves/min) both declined; the curves were biphasic with a plateau across hours 4-6. In contrast, the behavior of amplitude and incidence was strikingly different in dark period NREM sleep. At dark onset, amplitude increased sharply and remained at this elevated level without any significant trend across the 12 hours. Delta incidence was low at dark onset and increased with a strong linear trend. These data point to several experiments to test the mechanisms mediating the behavior of delta wave amplitude at the light-dark transition; they also bear on the homeostatic model of delta sleep.

Analysis of Variance↗
PubMed1993

Ketamine administration during waking increases delta EEG intensity in rat sleep.

Ketamine is known to increase the metabolic rate of limbic brain structures. We exploited this action to test a hypothesis of the homeostatic model of delta sleep: that an increase in the waking metabolic rate of plastic neuronal systems would increase delta electroencephalographic (EEG) intensity in subsequent nonrapid-eye-movement (NREM) sleep. In separate experiments, we gave intraperitoneal injections of ketamine to Sprague-Dawley rats of either 15, 25, or 50 mg/kg (0.055, 0.091, 0.18 mmol/kg) three times, at approximately hourly intervals, during the dark (waking) period; the last dose was given 4 to 5 hours before onset of the light (sleep) period. After ketamine, both NREM duration and delta EEG intensity (amplitude and incidence) increased significantly over control (saline injections) levels. The magnitude of this increase places it among the largest pharmacologically induced stimulations of delta sleep yet observed. The interpretation of this effect is complicated by the fact that ketamine produces widespread metabolic changes throughout the brain and it also acts on several receptor classes. However, since ketamine's major action is noncompetitive blockade of the cation channel gated by the N-methyl-D-aspartate receptor, our data join recent observations that suggest that excitatory amino acid receptor systems are involved in sleep regulation.

Animals↗
PubMed1993

A cortical EEG frequency with a REM-specific increase in amplitude.

1. We used period/amplitude (PA) analysis to survey electroencephalography (EEG) across vigilance states in the Sprague-Dawley rat. We found a fast cortical EEG frequency band, which we designate rho, whose wave amplitude in rapid eye movement (REM) was elevated above the levels in both waking and nonrapid eye movement (NREM). Rho wave amplitudes in NREM and waking were similar. 2. Rho occurred between 20 and 30 Hz, which appears to be a transitional range. In the 5-Hz band below rho, EEG wave amplitudes are higher in both NREM and REM than in waking; above 30 Hz, amplitudes are higher in waking and REM than in NREM. The augmented amplitude of rho in REM may result from a unique point of interaction of EEG mechanisms of sleep and waking. 3. In addition to its theoretical interest, rho is of practical value for scoring REM sleep. It could obviate the need to record hippocampal theta EEG, eliminating electrode penetration of the brain and reducing the number of leads required to classify rat vigilance states.

Animals↗
PubMed1993

Total sleep deprivation in the rat transiently abolishes the delta amplitude response to darkness: implications for the mechanism of the "negative delta rebound".

1. The homeostatic model of delta sleep has provided a useful framework for basic sleep research. This model is based on the relation of delta EEG to the duration of prior waking in man, a relation highlighted by the marked increase (rebound) in the delta EEG of nonrapid eye movement (NREM) sleep that follows total sleep deprivation (TSD). The generality of this model is severely challenged by the response to TSD in the rat. In the 12-h light period (LP) that immediately follows TSD, the rat shows a massive increase in REM sleep but only a modest increase in NREM delta EEG. Although this initial delta increase does not nearly compensate for the delta lost during deprivation, the rat then exhibits a depressed rate of delta production (the "negative delta rebound"). This robust and reproducible reaction worsens the delta deficit. 2. Using rats with chronic electrode implantations, we deprived them of all sleep for 24 h by handling them gently when they became inactive. We found that the negative delta rebound entails a transient, near-total failure of delta amplitude to increase normally in response to the onset of darkness. This loss of the rat's EEG response to darkness suggests a disruption of basic sleep physiology and raises the possibility that the negative rebound is also a pathological response. 3. We hypothesize that the negative rebound is maladaptive, and is caused by the massive increase in REM sleep that precedes it; this hypothesis can be tested experimentally.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Beta (20-28 Hz) and delta (0.3-3 Hz) EEGs oscillate reciprocally across NREM and REM sleep.

Across-night oscillations of beta (20-28 Hz) and delta (0.3-3 Hz) electroencephalograms (EEGs) were examined with spectral analysis in 10 normal young adult subjects (Ss). In each S, power densities of beta were found to oscillate reciprocally with delta power density across both nonrapid eye movement (NREM) and rapid eye movement (REM) sleep. Linear correlation coefficients between log power density of delta vs. beta were significant (p less than 0.0001) for each S. An incidental observation was that beta power within REM was reliably lower in epochs with more eye movement activity. The reciprocal relationship between beta and delta holds implications for sleep physiology and supplements our earlier finding that sigma (12-15 Hz) oscillates reciprocally with delta within NREM sleep. These descriptions of the continuously varying EEG across sleep provide information not available when EEG measures are tabulated by discrete NREM periods and REM periods.

Adolescent↗
PubMed1992

Precise conservation of NREM period 1 (NREMP1) delta across naps and nocturnal sleep: implications for REM latency and NREM/REM alternation.

The delta integrated amplitude (DIA) in nonrapid eye movement period 1 (NREMP1) of daytime naps was precisely subtracted from the NREMP1s of ensuing nocturnal sleep, indicating that the brain can retain a record of DIA expressed in sleep episodes initiated 12.5 and 8.5 hours before nocturnal sleep onset. The DIA subtraction was primarily accomplished by reduced NREMP1 duration [earlier rapid eye movement (REM) onset], suggesting that the timing of REM period 1 (REMP1) onset is controlled by delta need. This result is consistent with the hypothesis that REM sleep occurs when a stimulus for NREM has been partially depleted.

Adult↗
PubMed1991

Sigma (12-15 Hz) and delta (0.3-3 Hz) EEG oscillate reciprocally within NREM sleep.

Sleep EEG in the sigma and delta frequency bands was subjected to spectral analysis in 8 normal young adults. In each subject, power density of sigma and delta oscillated reciprocally during NREM sleep, confirming an observation made initially with period/amplitude analysis. In REM sleep, power density for both frequency bands was at its lowest levels. Correlation coefficients between power density of delta vs. 1/sigma for all artifact-free 20-s epochs of NREM sleep/night were highly significant for each subject. These results show that cyclic oscillation of EEG within sleep is not limited to delta frequencies. The reciprocal relation of sigma to delta holds implications for the EEG mechanisms of NREM sleep. This dynamic pattern may also prove useful for sleep stage scoring and for a finer empirical analysis of sleep in psychiatric and neurological disorders.

Activity Cycles↗
PubMed1991

Acute deprivation of the terminal 3.5 hours of sleep does not increase delta (0-3-Hz) electroencephalograms in recovery sleep.

Sleep electroencephalograms (EEG) and electrooculograms were recorded in nine young adult males on a baseline night, a night in which they were deprived of an average of 3 hr 27 min of sleep by early awakening, and on a recovery night. Records were analyzed by visual sleep stage scoring and period-amplitude analysis; the results of both were tabulated by successive nonrapid eye movement periods (NREMPs) and rapid eye movement (REM) periods. Neither visually scored delta nor REM measures were affected by this substitution of waking for sleep. Although there was a significant increase in the 0-3-Hz time/epoch on the recovery night, this finding was not confirmed in the accompanying report. These results, taken in association with data from previous studies, are consistent with the hypothesis that, in an acute experiment, visually scored delta and computer-measured 0-3-Hz EEGs increase above the baseline levels only if there has been loss of stage 3/4 EEG (or of sleep) from the first two NREMPs. The findings here are inconsistent with older reports and indicate that further parametric data are required to construct a quantitative model of the relation of sleep EEG waveforms to the duration of prior waking.

Adult↗
PubMed1991

Acute deprivation of the terminal four hours of sleep does not increase delta (0-3-Hz) electroencephalograms: a replication.

This experiment evaluated further our previous finding that substitution of waking for the terminal 3-4 hr of sleep produces little or no increase in either visually scored or computer measures of delta sleep. Eleven young adults (mean age 24.5 yr) were studied on a baseline night, a night with sleep limited to an average of 188 min, and a recovery night. Visually scored sleep stages, eye movement activity and computer measures of 0-3 Hz were analyzed by nonrapid eye movement periods (NREMPs) and for all recorded sleep in each condition. In addition, we measured the heights, durations and areas under the curve manifested by the cyclic waxing and waning of 0-3-Hz integrated amplitude across sleep. Acute loss of 3.9 hr of sleep did not increase either visual or computer measures of delta electroencephalograms (EEG) on the recovery night, essentially confirming our previous findings. We hypothesize that augmentation of delta EEG above baseline levels after acute (one night's) sleep loss requires that disruption or loss of sleep from the first two NREMPs (or delta cycles). Rapid eye movement (REM) sleep durations on the recovery night were unaffected by the marked loss of REM sleep caused by partial deprivation. Although eye movements as well as stage REM were lost in the deprivation condition, eye movement density was significantly reduced rather than increased on the recovery night. This reduction is consistent with the hypothesis that REM activity varies inversely with sleep depth (or directly with central arousal level). The observations here, taken in association with previous results, suggest that a threshold for eye movement suppression by sleep deprivation in young adults lies in the range of 3-4 hr of prior sleep loss.

Adult↗