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Biomedical subjects

R Stickgold

Publications and source records attributed to R Stickgold.

14 recordsLinked to original sources
PubMed1999

Sleep-induced changes in associative memory.

The notion that dreaming might alter the strength of associative links in memory was first proposed almost 200 years ago. But no strong evidence of such altered associative links has been obtained. Semantic priming can be used to quantify the strength of associative links between pairs of words; it is thought to measure the automatic spread of activation from a "node" representing one word to nodes representing semantically related words. Semantic priming could thus be used to test for global alterations in the strengths of associative links across the wake-sleep cycle. Awakenings from REM and nonREM (NREM) sleep produce a period of state carry-over during which performance is altered as a result of the brain's slow transition to full wakefulness, and cognitive testing in this period can provide information about the functioning of the brain during the prior sleep period. When subjects were tested across the night--before and after a night's sleep as well as immediately following forced awakenings from REM and NREM sleep--weak priming (e. g., thief-wrong) was found to be state dependent (p = 0.016), whereas strong priming (e.g., hot-cold) was not (p = 0.89). Weak primes were most effective in the presleep and REM sleep conditions and least effective in NREM and postsleep conditions. Most striking are analyses comparing weak and strong priming within each wake-sleep state. Contrary to the normal pattern of priming, subjects awakened from REM sleep showed greater priming by weak primes than by strong primes (p = 0.01). This result was seen in each of three protocols. In contrast, strong priming exceeded weak priming in NREM sleep. The shift in weak priming seen after REM sleep awakenings suggests that cognition during REM sleep is qualitatively different from that of waking and NREM sleep and may reflect a shift in associative memory systems, a shift that we hypothesize underlies the bizarre and hyperassociative character of REM-sleep dreaming. Known changes in brainstem activity that control the transition into and maintenance of REM sleep provide a possible explanation of this shift.

Adult↗
PubMed1998

The neuropsychology of REM sleep dreaming.

Recent PET imaging and brain lesion studies in humans are integrated with new basic research findings at the cellular level in animals to explain how the formal cognitive features of dreaming may be the combined product of a shift in neuromodulatory balance of the brain and a related redistribution of regional blood flow. The human PET data indicate a preferential activation in REM of the pontine brain stem and of limbic and paralimbic cortical structures involved in mediating emotion and a corresponding deactivation of dorsolateral prefrontal cortical structures involved in the executive and mnemonic aspects of cognition. The pontine brainstem mechanisms controlling the neuromodulatory balance of the brain in rats and cats include noradrenergic and serotonergic influences which enhance waking and impede REM via anticholinergic mechanisms and cholinergic mechanisms which are essential to REM sleep and only come into full play when the serotonergic and noradrenergic systems are inhibited. In REM, the brain thus becomes activated but processes its internally generated data in a manner quite different from that of waking.

Animals↗
PubMed1998

Eyelid movements and mental activity at sleep onset.

The nature and time course of sleep onset (hypnagogic) mentation was studied in the home environment using the Nightcap, a reliable, cost-effective, and relatively noninvasive sleep monitor. The Nightcap, linked to a personal computer, reliably identified sleep onset according to changes in perceived sleepiness and the appearance of hypnagogic dream features. Awakenings were performed by the computer after 15 s to 5 min of sleep as defined by eyelid quiescence. Awakenings from longer periods of sleep were associated with (1) an increase in reported sleepiness, (2) a decrease in the length of mentation reports, (3) a decrease in the frequency of reports of normal, wake-like thoughts, (4) an increase in the frequency of "unusual thoughts," and (5) increased frequencies of formal dream features, including visual hallucination, self-representation, fictive movement, narrative plot, and bizarreness. While sleep-onset reports can include all features of rapid eye movement (REM) dream reports, the number of such features is markedly reduced at sleep onset, suggesting that this mentation is a greatly diminished version of REM dreaming.

Adult↗
PubMed1998

To dream or not to dream? Relevant data from new neuroimaging and electrophysiological studies.

The study of sleep and dreams has enjoyed a major breakthrough with recent findings from brain imaging studies in humans. Several independent groups have shown global deactivation of the brain during non rapid eye movement sleep and a regionally selective reactivation during rapid eye movement sleep. These results are complemented by new brain lesion and electrophysiological recording data to give a detailed picture of the brain dynamics of changes in conscious state.

Brain Mapping↗
PubMed1997

The effect of optokinetic stimulation on daytime sleepiness.

This study examined the effect of optokinetic stimulation on objective sleepiness, as measured by the Multiple Sleep Latency Test (MSLT). The Nightcap, a portable sleep monitor, was used in a novel way to perform MSLTs, as well as record sleep in the home. Subjects wore the Nightcap for seven consecutive nights. On days 3 and 5 of the protocol, subjects came into the lab for an MSLT. On the experimental day, subjects underwent 10 minutes optokinetic stimulation (OKS), resulting in moderate motion sickness prior to each MSLT trial. Although subjects in the OKS condition reported significantly more drowsiness than controls, this did not result in significantly reduced sleep latencies.

Analysis of Variance↗
PubMed1996

Event-related potentials (ERPs) to deviant auditory stimuli during sleep and waking.

Using an oddball paradigm with two tones differing in pitch and probability, event-related potentials (ERPs) were compared during wake and two sleep stages. REM and NREM sleep stages were identified in nine subjects using the Nightcap which continuously records eye and body movements. The N1 occurred later and the P2 was larger during sleep than when awake. The N1 to the infrequent tones was larger during both sleep stages. A late negative wave was significantly larger to infrequent tones during REM sleep. It is concluded that representations of auditory stimuli occur in sleep, and most prominently during the REM phase. The prolonged latency of the ERP components indicates that processing of external sensory stimuli may be delayed.

Acoustic Stimulation↗
PubMed1995

Sleep. Sleep the beloved teacher?

Recent studies of humans and rats show that neuronal firing patterns initiated by prior sensory stimulation, and even learning, can occur during sleep. But what they tell us about the functions of sleep remains unclear.

Animals↗
PubMed1995

Nightcap: laboratory and home-based evaluation of a portable sleep monitor.

In this paper, we describe the first field tests of a home-based sleep monitoring system, the Nightcap, which uses eyelid and body movement sensors to discriminate wake, NREM, and REM sleep automatically. Ten normal young adults were studied in the sleep laboratory and at home to allow comparison of Nightcap-derived measures with those obtained by traditional polysomnography. The agreement between the two techniques was 87% based on 1-min epochs--93% for NREM, 80% for REM, and 72% for wake. When the values for sleep latency, REM latency, wake time, NREM time, and REM time calculated from polysomnograph records were compared with the values calculated from Nightcap data, no significant differences were seen. In cases of extremely poor sleep, objective sleep efficiency estimates correlated well with subjective reports, suggesting that the Nightcap is sensitive to clinically relevant changes in the quality of sleep. This new device should prove useful to researchers wishing to study the psychophysiology and pathophysiology of sleep in more naturalistic and cost-effective paradigms than possible in the traditional sleep laboratory.

Adult↗
PubMed1994

Nightcap measurement of sleep quality in self-described good and poor sleepers.

The Nightcap is a home-based sleep monitoring device that reliably differentiates rapid eye movement sleep, nonrapid eye movement sleep and wake states using eyelid and body movement measurements. This study documents its capacity to measure differences in sleep latency and sleep efficiency between self-described good and poor sleepers drawn from a normal population. Ten self-described "good" sleepers and 11 self-described "poor" sleepers were selected from a pool of college students. These groups differed significantly on selection parameters and on subjective estimates of sleep quality obtained each morning during the study. Each subject wore the Nightcap at home for 12-17 nights. Statistically significant differences in Nightcap-measured sleep latency and sleep efficiency were obtained between groups using individual subject means. In individual subjects, Nightcap measurements of sleep latency were correlated with subjective estimates of sleep latency. Poor sleepers were less accurate in estimating their sleep onset latency than were good sleepers. The demonstrated sensitivity of the Nightcap to good and poor sleep in these normal subjects augurs well for its application in a clinical setting.

Adult↗
PubMed1993

Suppression of eltoprazine-induced REM sleep rebound by scopolamine.

Previous studies have demonstrated that REM sleep suppression produced by the serotonin1 agonist eltoprazine (1 mg/kg b.i.d., administered i.p.) is followed by a dramatic rebound in REM sleep. In the present study, cats were treated with scopolamine (2 mg/kg b.i.d.) after 3 days of eltoprazine-induced REM sleep suppression. During scopolamine treatment, the percentage of REM sleep (9.9 +/- 3.5%) was well below baseline levels (13.7 +/- 1.6%; P < 0.05). Even after the 3-day scopolamine treatment ended, the subsequent REM sleep rebound after the combined eltoprazine-scopolamine treatment (16.8 +/- 2.8% REM sleep during 3-day rebound; P < 0.10 compared to baseline) was less than a third of the rebound normally seen after eltoprazine. These results provide evidence for the reciprocal relationship between acetylcholine and serotonin and suggest a new set-point model for the mechanism of REM sleep regulation and rebound.

Analysis of Variance↗
PubMed1977

Selective amplification of genes on the R plasmid, NR1, in Proteus mirabilis: an example of the induction of selective gene amplification.

The drug-resistance plasmid, NR1, is a 37-micron circular DNA molecule that contains two components: the resistance transfer factor (29 micron) carrying the transfer genes and the genes for tetracycline resistance, and the r-determinant (8 micron) carrying the genes for resistance to several other antibiotics including chloramphenicol (Cm). In Proteus mirabilis, these two components are capable of independent replication, or they may replicate as a composite molecule. When cells of P. mirabilis containing NR1 are cultured in medium containing Cm at 250 microgram/ml a growth lag of 20-35 hr ensues. During this lag, Cm induces the selective amplification of the r-determinant, including the gene for resistance to Cm. The amplification results from the excision of the r-determinant from the R plasmid, the independent replication of the r-determinant to give polymeric as well as monomeric r-determinants, and the eventual reintegration of multiple tandem copies of the r-determinant with the resistance transfer factor to form a new R plasmid with multiple copies of the r-determinant. This mechanism represents a new level of control of gene expression in bacterial systems--namely, the induction of selective gene amplification.

Cell Division↗
PubMed1977

Synaptic excitation and inhibition resulting from direct action of acetylcholine on two types of chemoreceptors on individual amphibian parasympathetic neurones.

1. Synaptic transmission was studied in visually identified parasympathetic ganglion cells that modulate the heart beat of the mudpuppy Necturus maculosus).2. The brief pulse of acetylcholine (ACh) released from terminals of the vagus nerve after each impulse can produce two distinct post-synaptic responses in individual principal cells of the ganglion: (i) within a milli-second of release, ACh generates a rapid and strong excitatory post-synaptic potential (e.p.s.p.) that normally initiates a post-synaptic impulse; (ii) this excitation is usually followed by a slow hyperpolarizing inhibitory post-synaptic potential (i.p.s.p.) that lasts for several seconds. The magnitude and time course of the i.p.s.p. depends on the frequency and number of vagal stimuli. When the hydrolysis of ACh is inhibited by prostigmine, a train of nerve stimuli may be followed by an i.p.s.p. lasting half a minute or longer.3. The rapid e.p.s.p. and slow i.p.s.p. result from the direct action of ACh on two different types of chemoreceptors in the post-synaptic membrane of the principal cell. The e.p.s.p. can be preferentially blocked by the nicotinic antagonist dihydro-beta-erythroidine (5 x 10(-7)M), while the i.p.s.p. is selectively blocked by the muscarinic antagonist atropine (5 x 10(-9)M).4. Potentials resembling nerve-evoked e.p.s.p.s and i.p.s.p.s can be produced by iontophoretic release of ACh from micropipettes onto the post-synaptic membrane. Application of the muscarinic agonist bethanechol generates exclusively inhibitory responses.5. The reversal potential for the i.p.s.p. is about -105 mV, which is approximately the equilibrium potential for potassium (E(K)). When the external K(+) concentration is altered, the reversal potential for inhibition is shifted to the new value of E(K) as expected from the Nernst equation. Changes in the external Na(+) and Cl(-) concentrations have no appreciable effect on the reversal potential. Thus, the i.p.s.p. is the result of a conductance increase for K(+).6. The conductance change producing the i.p.s.p. is voltage sensitive. When the membrane potential is shifted from -40 to -60 mV, the i.p.s.p becomes larger and longer. Beyond -60 mV the inhibitory response decreases in proportion to the driving force on K(+) without any further change in time course.7. The inhibitory response produced by an iontophoretically applied pulse of bethanechol has a delayed onset of about 150 msec at 24 degrees C. The early portion of this response, including the delay, is proportional to t(3), where t is time. The proportionality factor (the apparent rate constant) decreases elevenfold when the temperature is lowered by 10 degrees C. This suggests that a multi-step process is involved in the activation of the conductance increase that leads to the inhibitory response. Inhibitory responses with similar kinetics were produced in heart muscles of the mudpuppy upon application of ACh.

Acetylcholine↗
PubMedDate not supplied

Sleep and vestibular adaptation: implications for function in microgravity.

Optimal human performance depends upon integrated sensorimotor and cognitive functions, both of which are known to be exquisitely sensitive to loss of sleep. Under the microgravity conditions of space flight, adaptation of both sensorimotor (especially vestibular) and cognitive functions (especially orientation) must occur quickly--and be maintained--despite any concurrent disruptions of sleep that may be caused by microgravity itself, or by the uncomfortable sleeping conditions of the spacecraft. It is the three-way interaction between sleep quality, general work efficiency, and sensorimotor integration that is the subject of this paper and the focus of new work in our laboratory. To record sleep under field conditions including microgravity, we utilize a novel system called the Nightcap that we have developed and extensively tested on normal and sleep-disordered subjects. To perturb the vestibular system in ground-based studies, we utilize a variety of experimental conditions including optokinetic stimulation and both minifying and reversing goggle paradigms that have been extensively studied in relation to plasticity of the vestibulo-ocular reflex. Using these techniques we will test the hypothesis that vestibular adaptation both provokes and is enhanced by REM sleep under both ground-based and space conditions. In this paper we describe preliminary results of some of our studies.

Adaptation, Physiological↗