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J A Hobson

Publications and source records attributed to J A Hobson.

At least 37 records · Page 2Linked 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↗
PubMed1999

Parasomnias.

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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

Cholinergic and non-cholinergic afferents of the caudolateral parabrachial nucleus: a role in the long-term enhancement of rapid eye movement sleep.

A single microinjection of the cholinergic agonist carbachol into the feline caudolateral parabrachial nucleus produces an immediate increase in state-independent ipsilateral ponto-geniculooccipital waves, followed by a long-term rapid eye movement sleep enhancement lasting 7-10 days. Using retrogradely-transported fluorescent carbachol-conjugated nanospheres and choline acetyltransferase immunohistochemistry, afferent projections to this injection site for long-term rapid eye movement sleep enhancement were mapped and quantified. Six regions in the brain stem contained retrogradely-labelled cells: the raphe nuclei, locus coeruleus, laterodorsal tegmental nucleus, pedunculopontine tegmental nucleus, parabrachial nucleus, and the pontine reticular formation. The retrogradely-labelled (rhodamine+) cells in the pontine reticular formation and pedunculopontine tegmental nucleus contributed the predominant input to the parabrachial nucleus injection site (34.3 +/- 5.3% and 28.4 +/- 5.6%, respectively), compared to the laterodorsal tegmental nucleus (5.8 +/- 3.8%), parabrachial nucleus (13.5 +/- 3.1%), raphe nuclei (12.9 +/- 2.7%), and locus coeruleus (5.1 +/- 2.4%). By comparison with findings of afferent input to the induction site for short-latency rapid eye movement sleep in the anterodorsal pontine reticular formation, the parabrachial nucleus injection site is characterized by a similar proportion of afferents, except that the raphe nuclei were found to provide more than a two-fold greater input. Retrogradely-labelled neurons quantified in these nuclear regions consisted of 21.5% double-labelled (rhodamine+/choline acetyltransferase+) cholinergic and 78.5% noncholinergic (rhodamine+/choline acetyltransferase-) cells. The pedunculopontine tegmental nucleus contributed the predominant (51.7 +/- 8.2%) cholinergic input, compared to laterodorsal tegmental nucleus (20.7 +/- 10.2%), parabrachial nucleus (23.1 +/- 7.5%), and pontine reticular formation (4.4 +/- 2.1%). A comparative analysis of the total retrogradely-labelled cells within each nuclear region which were also double-labelled showed the highest proportion in the laterodorsal tegmental nucleus (76.2 +/- 7.5%) compared to pedunculopontine tegmental nucleus (39.4 +/- 3.6%), parabrachial nucleus (37.3 +/- 2.8%), and pontine reticular formation (3.2 +/- 2.1%). These data indicate that while pedunculopontine tegmental nucleus and laterodorsal tegmental nucleus neurons exert a powerful cholinergic influence on the injection site for long-term rapid eye movement enhancement, a major component of the afferent circuitry is non-cholinergic. Since the non-cholinergic input includes contributions from the locus coeruleus and raphe nuclei, it is probable that the caudolateral parabrachial nucleus contains cholinergic and aminergic afferent systems that participate in the long-term enhancement of rapid eye movement sleep.

Afferent Pathways↗
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↗
PubMed1998

Primary vagally mediated decelerations in heart rate during tonic rapid eye movement sleep in cats.

Rapid eye movement (REM) sleep results in profound state-dependent alterations in heart rate. The present study describes a novel phenomenon of a primary deceleration in heart rate that is not preceded or followed by increases in heart rate or arterial blood pressure and occurs primarily during tonic REM sleep. The goals were to characterize the primary decelerations and to provide insights on the underlying central and peripheral autonomic mechanisms. Cats were chronically implanted with electrodes to record electroencephalogram, pontogeniculooccipital wave activity in lateral geniculate nucleus, hippocampal theta rhythm, electromyogram, electrooculogram, respiration (diaphragm), and electrocardiogram. Arterial blood pressure was monitored from a carotid artery catheter. R-R interval fluctuations were continuously tracked using customized software. The muscarinic blocking agent glycopyrrolate (0.1 mg/kg i.v.) and the beta-adrenergic blocking agent atenolol (0.3 mg/kg i.v.) were administered in alternating sequence with a 90- to 120-min interval. Glycopyrrolate immediately eliminated the decelerations during REM sleep. Atenolol alone had no effect on their frequency. These findings suggest that a change in the centrally induced pattern of autonomic activity to the heart is responsible for the primary decelerations, namely, a bursting of cardiac vagal efferent fiber activity.

Adrenergic beta-Antagonists↗
PubMed1997

Consciousness in waking and dreaming: the roles of neuronal oscillation and neuromodulation in determining similarities and differences.

State-dependent aspects of consciousness are explored with particular attention to waking and dreaming. First, those phenomenological differences between waking and dreaming that have been established through subjective reports are reviewed. These differences are robustly expressed in most aspects of consciousness including perception, attention, memory, emotion, orientation, and thought. Next, the roles of high frequency neuronal oscillation and neuromodulation are explored in waking and rapid eye movement sleep, the stage of sleep with which the most intense dreaming is associated. The high frequency neuronal oscillations serve similar functions in the wake and rapid eye movement states sleep but neuromodulation is very different in the two states. The collective high frequency oscillatory activity gives coherence to spatially separate neurons but, because of the different neuromodulation, the binding of sensory input in the wake state is very different from the binding of internally perceived input during rapid eye movement sleep. An explanatory model is presented which states that neuromodulation, as well as input source and brain activation level differentiate states of the brain, while the self-organized collective neuronal oscillations unify consciousness via long range correlations.

Consciousness↗
PubMed1997

Dreaming as delirium: a mental status analysis of our nightly madness.

Dreaming is characterized by formal visual imagery (akin to hallucination), by inconstancy of time, place, and person (akin to disorientation), by a scenario-like knitting together of disparate elements (akin to confabulation), and by an inability to recall (akin to amnesia). Taken together, these four dream features are similar to the delirium of organic brain disease. By studying the brain during rapid-eye-movement (REM) sleep-the phase of sleep in which most dreaming occurs-we can begin to understand its basis in the altered neurophysiology of REM.

Brain↗
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↗
PubMed1996

How the brain goes out of its mind.

Dreaming is characterized by formal visual imagery (akin to hallucination), by inconstancy of time, place and person (akin to disorientation), by a scenario-like knitting together of disparate elements (akin to confabulation) and by an inability to recall (akin to amnesia). Taken together, these four dream features are similar to the delirium of organic brain disease. By studying the brain during rapid-eye-movement (REM) sleep--the phase of sleep in which most dreaming occurs--we can begin to understand its basis in the altered neurophysiology of REM.

Amnesia↗
PubMed1996

Physical motion in dreams: one measure of three theories.

As a normal psychological event, dreaming is an object of fascination and of conflicting explanation. In biopsychological terms, this article compares 3 explanations of 1 salient feature of dream cognition. Physical movement can be measured in dream reports, can be understood in physiologic terms, and can provide a focus for comparing dream theories. In addition, dreamed motion may have functional importance. The authors discuss dream motor data that conflict with Freud's explanation of dream movement and with a distributed activation explanation but coincide with an activation-synthesis hypothesis. Because physiologic models of sleep intersect with physiologic models of psychopathology, this approach may be relevant to psychopathological dreaming.

Arousal↗
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

Suppression of ponto-geniculo-occipital waves by neurotoxic lesions of pontine caudo-lateral peribrachial cells.

Ponto-geniculo-occipital waves precede rapid eye movement sleep and play an important role in triggering and maintaining rapid eye movement sleep. Ponto-geniculo-occipital waves have been implicated in several important functions such as sensorimotor integration, learning, cognition, development of the visual system, visual hallucination, and startle response. Peribrachial area neurons have long been thought to play a key role in the triggering of ponto-geniculo-occipital wave. However, the exact location within the peribrachial area for triggering pontine ponto-geniculo-occipital wave has not been unequivocally demonstrated. In an attempt to address this issue, kainic acid was microinjected (1.0 micrograms) unilaterally into the caudo-lateral peribrachial area of four cats in order to destroy the cell bodies located in that region and thus to study the effects of their destruction upon waking-sleep states and ponto-geniculo-occipital waves. The kainic acid produced a small spherical area of nerve cell loss and/or gliosis centered on the stereotaxic coordinates of P: 4.0, L: 4.5, and H: -2.5. The maximum diameter of that spherical area of cell loss was 0.9 mm. Unilateral lesioning of the caudo-lateral peribrachial area decreased ponto-geniculo-occipital waves during rapid eye movement sleep by 85% ipsi-laterally and 15% contralaterally in the lateral geniculate body without significantly changing the amounts of time spent in wake, slow-wave sleep, and rapid eye movement sleep. These results suggest that the caudo-lateral peribrachial area cells are critical to the genesis of ponto-geniculo-occipital waves, and provide compelling evidence that the different parts of the peribrachial area have quite different roles in the generation of discrete rapid eye movement sleep signs. We propose that caudo-lateral peribrachial cells exert an excitatory influence on rostral peribrachial cells, which then directly activate the ponto-geniculo-occipital waves that are recorded in the lateral geniculate body. Results of this study are not only important to understand the mechanisms generating ponto-geniculo-occipital waves but also could be used as an experimental tool to study the functions of this wave.

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↗