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Biomedical subjects

J A Hobson

Publications and source records attributed to J A Hobson.

At least 19 recordsLinked to original sources
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↗
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↗
PubMed1994

Neuronal activity in the caudolateral peribrachial pons: relationship to PGO waves and rapid eye movements.

1. The present study was performed to examine the hypothesis that the caudolateral peribrachial area (C-PBL) may be directly involved in shifting the brain from the nonpontogeniculooccipital (non-PGO)-related states of waking (W) and slow-wave sleep (S) to the PGO-related states of slow-wave sleep with PGO waves (SP) and rapid eye movement (REM) sleep. 2. To test this hypothesis at the cellular level, we have recorded a sample of 226 spontaneously discharging units of the C-PBL during natural sleep-waking cycles in unanesthetized head-restrained cats and have correlated the action-potential data with the PGO waves. 3. Of these 226 cells, 67.26% (n = 152) were called PGO state-on units because they increased or began firing 15-5 s before the first PGO wave of SP and maintained their high firing rate throughout SP (31.30 +/- 6.0 Hz, mean +/- SD) and REM sleep (39.46 +/- 6.70 Hz); their firing rates in W (0.45 +/- 0.85) and S (0.70 +/- 1.26) were much lower. Among these PGO state-on neurons, 28.94% (n = 44) discharged high-frequency (> 500 Hz) spike bursts on the background of tonically increased firing rates during the PGO-related states. Contrastingly, 14.16% (n = 32) of the cells (called PGO state-off units) fired tonically during W (11.54 +/- 4.15) and S (9.43 +/- 3.87) but stopped or decreased firing 25-15 s before the first PGO wave of SP; their activity remained suppressed throughout SP (0.19 +/- 0.44) and REM sleep (0.03 +/- 0.17). The remaining 18.58% (n = 42) cells fired (9-10 Hz) tonically but were unrelated to the wake-sleeping cycle. 4. During SP and REM sleep, primary PGO waves were found to appear with equal frequency in each lateral geniculate body (LGB). During REM sleep these primary waves were ipsilateral to the direction of phasic rapid eye movements as previously reported by Nelson et al. (1983). 5. During SP and REM sleep PGO state-on burst cells fired high-frequency bursts on a background of tonic activity in association with each ipsilateral primary LGB PGO wave. The first spike of a burst preceded the beginning of the negative component of the ipsilateral LGB PGO waves by 25 +/- 7.5 ms. On the basis of their sustained firing and the latency of their PGO-related bursting, we call these neurons long-lead PGO-on burst-tonic cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
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↗
PubMed1993

Osseointegrated implants in the management of childhood ear abnormalities: the initial Birmingham experience.

Over a four-year period 72 children with ear abnormalities have been referred for assessment by the extraoral osseointegrated implant team at The Queen Elizabeth Hospital, Birmingham. Thirty-two children have been judged suitable for rehabilitation. Twelve children have completed rehabilitation using bone-anchored hearing aids and/or auricular prostheses. Two fixtures (seven per cent of those loaded) have dislodged and required replacement. Audiological assessment of the bone-anchored hearing aid users shows only small improvements in their aided thresholds, compared to thresholds obtained with their previous aid. However all now have thresholds of 30 dB(A) or better and report a marked improvement in sound quality. When surveyed, hearing aid and prosthesis users report high levels of satisfaction with this form of rehabilitation. The technique adds a new dimension to the management of children with aural anomalies. The approach and results of a multidisciplinary programme are reported.

Adolescent↗
PubMed1993

Dose-related suppression of REM sleep and PGO waves by the serotonin-1 agonist eltoprazine.

Parental administration of the serotonin-1 agonist eltoprazine (0.0625 to 4.0 mg/kg [0.0002 to 0.016 mmol/kg]) in freely moving cats produced significant suppression of electrophysiologic rapid eye movement (REM) sleep signs, ponto-geniculo-occipital (PGO) activity, and REM sleep behavior. The virtual total suppression of REM sleep (0.4%, 4.0 mg/kg) and PGO wave activity (2 to 4 mg/kg) in exchange for increasing amounts of non-REM (NREM) slow-wave sleep was a dose-dependent function of the amount of eltoprazine administered. Wakefulness was unaffected by eltoprazine regardless of dose. Concurrent with this dose-dependent suppression of REM was a dose-dependent increase in electroencephalographic synchrony and mean electromyographic amplitude. Since eltoprazine was found to shift the balance between REM and NREM sleep but did not change the balance between sleep and waking, it is a potentially useful tool for the investigation of serotonergic-cholinergic interaction.

Animals↗
PubMed1993

Effect of specific muscarinic M2 receptor antagonist on carbachol induced long-term REM sleep.

Six cats were chronically implanted with a standard set of sleep-scoring electrodes and bilateral stainless-steel guide tubes for microinjection of drugs in the peribrachial area (PBL). Pretreatment of drug injection sites in the PBL with the M2 antagonist methoctramine blocks both the immediate triggering of ponto-geniculo-occipital (PGO) waves and the later prolonged enhancement of REM sleep that is induced by carbachol. These results support the hypothesis that the carbachol effects are mediated via the M2 muscarinic receptor that is known to be present in the PBL.

Animals↗
PubMed1992

Sleep and dreaming: induction and mediation of REM sleep by cholinergic mechanisms.

The most important recent work on the neurobiology of sleep has focused on the precise cellular and biochemical mechanisms of rapid eye movement sleep mediation. Direct and indirect evidence implicates acetylcholine-containing neurons in the peribrachial pons as critical in the triggering and maintenance of rapid eye movement sleep. Other new studies provide support for the hypothesis that the cholinergic generator system is gated during waking by serotonergic and noradrenergic influences. A growing consensus regarding the basic neurobiology has stimulated new thinking about the brain basis of consciousness during waking and dreaming.

Acetylcholine↗
PubMed1992

Cholinergic microstimulation of the peribrachial nucleus in the cat. I. Immediate and prolonged increases in ponto-geniculo-occipital waves.

The cholinergic agonist carbachol was injected into the pontine Pb area where PGO bursting cells have been recorded. When microinjections were localized to the ventrolateral aspect of the caudal Pb nucleus near aggregates of ChAT immunolabeled cholinergic neurons, carbachol produced an immediate onset of state-independent PGO waves in the ipsilateral LGB. These state-independent PGO waves persisted for 3-4 days. After the first 24 hrs PGO wave activity increasingly became associated with REM sleep and with REM transitional SP sleep as both of these PGO-related states increased in amount to 3-4 times baseline levels. The increase in amount of PGO-related states peaked on days 2-4 following one carbachol injection and persisted for 10-12 days. These results suggest a two stage process: stage one, PGO enhancement, is the direct consequence of the membrane activation of cholinoceptive PGO burst neurons by carbachol; stage two, REM enhancement, is the consequence of metabolic activation of endogenous cholinergic neurons. This experimental preparation is a useful model for the study of the electrophysiology and functional significance of PGO wave and REM sleep generation.

Acetylcholine↗
PubMed1992

Cholinergic microstimulation of the peribrachial nucleus in the cat. II. Delayed and prolonged increases in REM sleep.

The hypothesis that REM sleep is cholinergically mediated is supported by the identification of a cholinoceptive trigger zone in the FTG. Since this trigger zone is devoid of cholinergic neurons, the aim of the present study was to test the hypothesis that a cholinergic drive for REM sleep may come from the cholinergic cells of the PBL region. Chronically implanted freely moving cats with electrodes for sleep and PGO wave recordings were used. Guide tubes were implanted for carbachol microinjections (4 micrograms/250 nl) in the PBL and FTG. All microinjections were delivered in close vicinity of ChAT+ cholinergic cells in the PBL region. Results showed that a single unilateral carbachol microinjection into the PBL induced sustained (24 hr) state-independent ipsilateral PGO wave activity. This PGO wave activity was followed by a prolonged enhancement of REM sleep lasting for more than six days. We also observed that REM enhancement was followed by a delayed but marked enhancement of S sleep episodes with PGO waves (SP), which are normally brief transitions from S to REM sleep. Our findings strongly support the hypothesis that cholinergic drive for REM sleep comes from the lateral pontine tegmentum and we suggest that the PBL region plays a major role in both PGO wave generation and long-term regulation of REM sleep induction.

Acetylcholine↗