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Biomedical subjects

J A Hobson

Publications and source records attributed to J A Hobson.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1992

Dynamic suppression of REM sleep by parenteral administration of the serotonin-1 agonist eltoprazine.

The purpose of this study was to determine the effects of the serotonin-1 agonist eltoprazine on the control of rapid eye movement (REM) sleep. Continuous polygraph recordings were performed for 15-17 days in four adult male cats. During the first 5 control days cats received injections of 0.9% saline intraperitoneally (i.p.) twice per day (b.i.d.). Over the next 5-7 days cats received injections of 0.9% saline intraperitoneally (i.p.) twice per day (b.i.d.). Over the next 5-7 days cats received eltoprazine i.p. (1-2 mg/kg, b.i.d.). For the final 5 recovery days cats received saline alone. During the saline control period, the mean REM sleep percent was 13.8 +/- 0.91%. When eltoprazine was administered for the subsequent 5-7 days, the mean REM percent was reduced to 1.5 +/- 0.59%. During the 5-day recovery period, REM percent increased significantly (p less than 0.0001) above both control and drug injection values to a mean of 24.5 +/- 1.3% with a maximum on recovery day 1 of 28.4 +/- 2.6% (n = 4). In addition to REM suppression, eltoprazine produced other electroencephalographic changes: an increase in slow-wave sleep (S) percent without any change in overall wake (W) percent; an increase in electromyogram (EMG) amplitude; and a decrease in ponto-geniculo-occipital (PGO) wave activity. PGO wave frequency and REM% increased significantly during the recovery period. Thus our findings demonstrate REM and PGO suppression by eltoprazine and document dramatic rebound effects following its withdrawal.

Animals↗
PubMed1991

Automated staging of sleep in cats using neural networks.

Manual staging of sleep based on visual EEG criteria is a laborious and time-consuming task. In an effort to automate sleep staging, we have developed a neural network that 'learns' to stage sleep on the basis of wave band count data alone, in the cat. Wave band count data are collected on a microcomputer, using period-amplitude analysis. Delta waves, spindle bursts, ponto-geniculo-occipital (PGO) waves, electro-oculogram (EOG), basal electromyogram (EMG) amplitude, and movement artifact amplitude are collected, and used to 'train' the network to score sleep. These wave count data serve as the input patterns to the net, and the corresponding manually scored sleep stages serve as a 'teacher.' We demonstrate that, when used to score the states of wake, slow wave sleep (SWS), desynchronized sleep (D), and the transition period from SWS to D (SP), these neural networks agree with manual scoring an average of 93.3% for all epochs scored. Neural network programs can learn both rules and exceptions, and since the nets teach themselves these rules automatically, a minimum of human effort is required. Because programming requirements are small for neural nets, this approach is readily adaptable to microcomputer-based systems and is widely applicable to both animal and human EEG analyses. The utility of this approach for the detection and classification of a variety of clinical neurophysiological disorders is discussed.

Animals↗
PubMed1991

Developmental phases of sleep and motor behaviour in a cat mother-infant system: a time-lapse video approach.

The evolution of sleep patterns in developing kittens was studied using time-lapse video technology and direct observation. The duration, frequency, and onset of the behavioural states and interactions of the cats were analyzed and then organized into phases that represent major changes in developmental structure during the first 6 weeks of kitten life. We have demonstrated that the kittens began exhibiting adult bi-cyclic sleep patterns on approximately Day 30 of development. During the 10-day period that preceded this consolidation of sleep pattern, REM sleep decreased by half, with a reciprocal increase in NREM sleep. These changes were coincident with an increase in kitten patterned motor behaviour and an increase in stimulation of the kittens by the mother during her bi-cyclic active periods.

Animals↗
PubMed1991

Long-term enhancement of REM sleep following cholinergic stimulation.

A six day long increase in rapid eye movement (REM) sleep followed the unilateral microinjection of a single dose of the cholinergic agonist drug carbachol into the brain stem of cats. Effective drug injection sites were localized to the pontine peribrachial region containing cholinergic choline acetyltransferase (ChAT) labeled neurons. At the peak of the effect, which occurred 24-28 h post-injection, the relative amount of time devoted to REM sleep tripled, resulting in an absolute time increase from 3.12 to 11.28 h REM sleep per day. This pronounced and prolonged REM sleep increase was associated with marked enhancement of ponto-geniculo-occipital (PGO) waves and with PGO burst cell activity unilateral to the site of injection.

Analysis of Variance↗
PubMed1990

A cholinoceptive desynchronized sleep induction zone in the anterodorsal pontine tegmentum: locus of the sensitive region.

Carbachol, a long-acting cholinergic agonist, was microinjected (4 micrograms/250 nl per 90 s) into 90 sites within the anterodorsal pontine tegmentum of four cats and the time to onset and percentage of time spent in a desynchronized sleep-like state during 40 min postinjection were calculated. Compared with more posteroventral pontine sites, the shorter latencies and higher percentages observed confirmed earlier predictions of a sensitive cholinoceptive zone in the anterodorsal pons. In 27 trials a desynchronized sleep-like state was observed within 5 min; in 31 trials the latency was 5-10 min and in the remaining 32 trials, greater than 10 min. Plotting the desynchronized sleep-like state latency and the desynchronized sleep-like state percentage as a function of the three-dimensional coordinates revealed that injection sites with short latency (less than 5 min) and high percentage (greater than 80%) were concentrated between the coordinates of P 1.0 to 3.5 and V -3.5 to -5.5, at the lateral coordinate L 2.0. On the frontal plane, the short desynchronized sleep-like state latency and high desynchronized sleep-like state percentage sites begin in the pontine tegmental region just lateral to the ventral tegmental nucleus and extend 3 mm ventrocaudally. A regression plot of the data in sagittal plane 2.0 revealed a short latency axis, around which the short latency sites cluster, running in a slightly dorsoventral direction from about P 1.0 to V -4.0 to P 4.0 to V -5.5. This observation suggests that the sensitive zone might approximate a cylinder in shape, a hypothesis supported by the correlation of longer latencies and lower percentages at increasing radial distance from the axis. The non-linear relationship between cholinergic potency and distance from the short latency axis suggests that the desynchronized sleep-like state latency is a function of two factors; a variable diffusion-based delay of carbachol to distant neuronal populations involved in the desynchronized sleep-like state production, and a fixed recruitment-based delay following activation of neurons in the sensitive zone. Interpretation of these findings in light of earlier studies involving microstimulation of the pontine tegmentum argue in favor of a distributed network of discrete neuronal populations as the source of desynchronized sleep generation.

Animals↗
PubMed1990

A cholinoceptive desynchronized sleep induction zone in the anterodorsal pontine tegmentum: spontaneous and drug-induced neuronal activity.

The effect of carbachol microapplication (4 micrograms/250 nl per 90 s) on the discharge of neurons in the anterodorsal pons of four cats was studied using a newly devised microinjector-microelectrode assembly. Neurons were classified according to the magnitude of their discharge rate increases (or decreases) in physiological desynchronized sleep as desynchronized-on (or desynchronized-off) before injecting carbachol. When carbachol produced a desynchronized sleep-like state only half (15 out of 30) of the desynchronized-on cells were activated (desynchronized-on/desynchronized sleep-like state-on) while the other half were not (desynchronized-on/desynchronized sleep-like state-not on). Compared with the non-activated cells, the desynchronized-on/desynchronized sleep-like state-on cells had three features consistent with playing an active role in desynchronized sleep generation: these cells had a higher mean discharge frequency in desynchronized sleep and higher ratio of discharge frequency in desynchronized sleep compared with wakefulness; they did not fire in phase with electromyogram excitation of neck muscles; and they were concentrated in the short latency desynchronized sleep-like state induction zone described in the companion paper. The three-way correlation between the optimal anatomical site for short latency desynchronized sleep-like state induction, the selective neuronal discharge pattern in desynchronized sleep and the cholinergic activation pattern in the desynchronized sleep-like state suggest that we may have identified a neuronal population that is cholinoceptively activated as part of the physiological mechanism of desynchronized sleep generation.

Activity Cycles↗