Showing papers on "Rapid eye movement sleep published in 1977"

Pontine reticular formation neurons: relationship of discharge to motor activity

Abstract: The discharge correlates of pontine reticular formation units were investigated in unrestrained cats. In agreement with previous investigations using immobilized preparations, we found that these cells had high rates of activity in rapid eye movement sleep, and responded in waking to somatic, auditory, and vestibular stimuli at short latencies, many having polysensory responses and exhibiting rapid "habituation." However, despite the sensory responses of these cells, most unit activity could not be explained by the presence of sensory stimuli. Intense firing occurred in association with specific movements. Units deprived of their adequate somatic, vestibular, and auditory stimuli showed undiminished discharge rates during motor activity. Discrete sensory stimuli evoked sustained unit firing only when they also evoked a motor response. We conclude that activity in pontine reticular formation neurons is more closely related to motor output than to sensory input.

Gating of neuronal transmission in the hippocampus: efficacy of transmission varies with behavioral state

Abstract: Electrical stimuli were applied to the angular bundle of the freely moving rat, and the neuronal responses were recorded ipsilaterally in the dentate gyrus and the CA1 field of the hippocampus. The number of neurons responding monosynaptically in the dentate gyrus was relatively small when the animal was alert and not moving but was much greater both during slow-wave sleep and during rapid eye movement sleep. In Ca1, however, the trisynaptic population response was considerably smaller during rapid eye movement sleep and when the animal was alert than during slow-wave sleep. These findings are interpreted in terms of a set of behaviorally dependent "neural gates". Measurement of the synaptic current at the dentate gyrus induced monosynaptically by stimulation of the angular bundle further suggests that the mechanism by which gating occurs at this level is either a tonic inhibitory synaptic influence exerted upon the granule cells during the alert state, a tonic excitatory influence during slow-wave sleep, or both.

Rapid eye movement sleep, motoneurone inhibition, and apneic spells in preterm infants.

Abstract: Summary: Not principally different from the results obtained in more mature subjects, monosynaptic reflex excitability of spinal motoneurones in preterm infants decreases during active sleep. However, in preterm infants the electric reflex response is not abolished, and is not even continuously depressed during the entire active sleep period. Spinal motoneurone inhibition is demonstrable only during certain periods of active sleep, and it is during this state of decreased spinal motoneurone excitability when apneic spells predominantly occur. Speculation: The concept of apneic spells being promoted by rapid eye movement (REM) sleep brain mechanisms, as outlined by Gabriel el al. (10) and supported by data of this study, can so far mainly explain respiratory pauses in otherwise healthy preterm infants. However, in neonatal sepsis, meningitis, hypoxia, hypoglycemia, etc., the same central nervous system inhibitory processes should increase the risk of apneic spells, provided that active sleep states still exist. Furthermore, Bryan and Bryan (2) have demonstrated a considerable thoracic wall instability during active sleep, which is probably also due to inhibition of spinal motoneurones innervating intercostal muscles. Thus, when respiratory brain stem centers are partly damaged, tonic spinal motoneurone inhibition during active sleep can additionally increase the infant's difficulty in maintaining sufficient respiration.

Cannabis, catecholamines, rapid eye movement sleep and aggressive behaviour.

Abstract: 1. Previous work from our laboratory has shown that cannabis induces aggressive behaviour in rats that have been deprived of rapid eye movement (REM) sleep. It was suggested that this effect was related to brain catecholamines, with dopamine playing an agonist role and noradrenaline an inhibitory one. The present paper describes new experiments dealing with this subject. 2. Previous REM sleep-deprivation enhanced both delta9-tetrahydrocannabinol (THC)-induced hypothermia and nomifensine effects on aggressive behaviour. 3. A marihuana extract decreased brain dopamine turnover in REM sleep-deprived rats, an effect not observed in non-deprived rats. Noradrenaline metabolism was not altered. 4. Fighting behaviour was elicited in REM sleep-deprived rats treated with 4 different dopamine-beta-hydroxylase inhibitors. 5. Apomorphine, nomifensine and delta9-THC administered to non-deprived rats pretreated with bis(4-methyl-1-homopiperanzinyl-thiocarbonyl) disulphide (Fla-63), induced fighting behaviour. 6. Nomifensine and apomorphine induced fighting in non-deprived rats pretreated with delta9-THC. 7. Clonidine inhibited the fighting elicited in REM sleep-deprived rats by either delta9-THC or Fla-63 pretreatment. 8. The data are discussed in terms of the influence of REM sleep-deprivation (or the stress associated with deprivation) on the response to dopaminergic drugs and cannabis. Taken together they emphasize the participation of brain dopamine and noradrenaline systems in the aggressive behaviour studied.

Rapid eye movement sleep, apnea, and cardiac slowing influenced by phenobarbital administration in the neonate.

Abstract: Polygraphic recordings were performed in seven preterm infants who had been given phenobarbital (phenobarbitone) to evaluate its effect on neonatal sleep behavior and on the incidence of neurogenic apnea and/or bradycardia. The amount of active sleep, as well as the incidence of apnea and/or cardiac slowing occurring predominantly in active sleep, were decreased at therapeutic serum levels of phenobarbital. With declining serum drug levels, active sleep showed a rebound effect; at the same time, apnea and/or cardiac slowing relapsed. Thus, our previously proposed neurophysiologic concept that neonatal apnea is facilitated by active sleep-inhibitory brain mechanisms seems to be confirmed.

Cocaine effects on sleep parameters in the rat.

Abstract: Cocaine in 6 mg/kg doses was administered orally and intraperitoneally to rats and sleep EEG's recorded. Cocaine significantly reduced total sleep time, slow-wave sleep, and sleep latency. Rapid eye movement sleep (REM) was significantly suppressed during the first half of the sleep recording. These effects were evident by both routes of administration. The effects of cocaine on total sleep time in animals parallels that observed in man.

Neuronal activity patterns during rapid-eye-movement sleep: relation to waking patterns

Abstract: Neuronal unit spike activity as detected by extracellular electrodes has been studied during waking, slow wave sleep (SWS) and rapid-eye-movement sleep (REMS) in a variety of brain sites. A consistent finding has been that a majority of cell types exhibit an increased neuronal discharge rate in REMS and in waking when compared with SWS. Indeed, REMS rates usually equal or exceed waking rates, and REMS has been described as a state characterized by intense excitation of brain unit activity. This observation, first reported by Huttenlocher (1961) for medial midbrain cells, has been extended to the cerebral cortex (Evarts, 1962, 1964; Noda & Adey, 1970), thalamus (Sakakura, 1968; Mukhametov, Rizzolotti, &Seitun, 1970; Mukhametov, Rizzolotti, & Tradardi, 1970), certain limbic sites (Noda, Manohar, & Adey, 1969; Findlay & Hayward, 1969) and most brainstem neurons (Kasamatsu, 1970; Bizzi, Pompeiano, & Somogyi, 1964; Hobson & McCarley, 1971). Other cell types have been found to exhibit reduced activity in REMS compared with SWS, but a similar reduction also occurs during waking, that is, the REMS-waking similarity applies (Jacobs S McGinty, 1971). Initially, these observations were interpreted as supporting concepts that SWS and REM sleep were dissimilar states and that sleep did not constitute