Mechanisms Of Paradoxical Sleep Research Articles

Effects of Electrical Stimulation of the Posterior Part of the Hypothalamus on the Spike Activity of Neurons in the Oral Nucleus of the Pons

Chronic experiments were performed on four cats to study evoked spike activity in neurons in the oral nucleus of the pons to electrical stimulation of the posterior hypothalamus in the waking, slow-wave sleep, and paradoxical sleep states. A total of 42% of study neurons were found to respond to stimulation during waking. PS-on and PS-off neurons were identified in the oral nucleus of the pons, along with phasic cells showing bursts of activity during the physical manifestations of paradoxical sleep. Stimulation induced inhibitory responses in PS-on neurons, excitatory responses in PS-off neurons, and excitatory and inhibitory responses in 68% and 32% respectively of phasic neurons. The magnitudes of evoked responses in these neurons changed during the sleep-waking cycle. These data demonstrate the involvement of the posterior hypothalamus in controlling the mechanisms of paradoxical sleep, these mechanisms being located in the oral nucleus of the pons.

Dynamics of neuron spike activity in the oral nucleus of the pons during the sleep-waking cycle in cats.

Chronic experiments on five cats were performed to study the spike activity of neurons in the oral nucleus of the pons during waking, slow-wave sleep, and paradoxical sleep. Groups of neurons with different dynamics of spike frequency were identified. Cells with rare discharges during waking and slow-wave sleep and maximum spike frequencies in the phasic stage of paradoxical sleep were regarded as PS-on neurons. Cells discharging at maximum frequency during waking, with decreases in frequency during slow-wave sleep and further decreases in paradoxical sleep, were regarded as PS-off neurons. Cells showing decreases in discharge frequency on the transition from waking to slow-wave sleep and increases in discharge frequency in paradoxical sleep, with grouped spikes during oculomotor activity, appeared to be responsible for generating the phasic phenomena of paradoxical sleep. The question of the involvement of neurons of different populations in the mechanisms of paradoxical sleep is discussed.

The role of the medial preoptic area of the hypothalamus in organizing the paradoxical phase of sleep.

Chronic experiments were performed on cats to study the effects of electrical stimulation of the medial preoptic area of the hypothalamus on the latent period, duration, and structure of paradoxical sleep, as well as the dynamics of neuron activity in this structure during the sleep-waking cycle. These investigations showed that low-frequency stimulation of the medial preoptic area during slow-wave sleep led to short-latency development of desynchronization of bioelectrical activity in the neocortex and initiated the development of paradoxical sleep or a similar state. Stimulation of this structure during paradoxical sleep led to a decrease in its duration, to the virtually complete disappearance of the tonic stage of paradoxical sleep, and to an increase in the frequency of rapid eye movements in the phasic stage. Rearrangement of neuron activity in the medial preoptic area during the sleep-waking cycle was similar to that seen in cells of the lower brainstem "executive" centers of paradoxical sleep. It is suggested that neurons in the medial preoptic area of the hypothalamus are actively involved in the mechanisms of paradoxical sleep and, in particular, in the desynchronization of neocortical bioelectrical activity which develops during this stage.

Paradoxical Sleep — A Study of its Nature and Mechanisms

This chapter discusses the results of a study that analyzes the nature and mechanisms of paradoxical sleep (P.S.), or rhombencephalic phase of sleep. In this study, both tonic and phasic electroencephalogram (EEG)or peripheral index of P.S. are very different from EEG and behavioral slow sleep. The pontine origin of rapid eye movements and of the phasic ponto-geniculo-occipital activity occurring during P.S. is emphasized. Phylogenetic study shows that slow sleep may be observed in reptiles, birds, and mammals. In contrast, P.S. is not found at all in the tortoise, and is of very short duration in birds (its ratio to the total sleep being only 0.2%). In mammals, this ratio is about 6–30%. Ontogenetic studies in the kitten show that P.S. may appear immediately after wakefulness and constitutes 90% of total sleep during the first days. In chronic pontile animals, with hypothalamic islands, the rhombencephalic phase of sleep, showing all the pontine electrical and behavioral criteria of P.S. in the intact animal, can be completely identified with the latter. Its mean duration (6 min) is analogous to that of the intact animal. No behavioral or EEG index of slow sleep was observed in pontile animals.

MECHANISMS OF PARADOXICAL SLEEP AS REVEALED BY NEUROPHYSIOLOGIC AND PHARMACOLOGIC APPROACHES IN THE RABBIT.

With the use of the Computer of Average Transients a study has been made of evoked responses in the central nervous system (CNS) of rabbits during paradoxical sleep and other stages of sleep and alertness. In “chronically implanted” animals responses evoked in the frontal cortex by stimulating the midbrain reticular formation were averaged and used as a guide to the state of wakefulness. During the alert state the averaged evoked responses show consistently a major peak at a latency of about 20–25 msec, which disappears during ordinary sleep. During paradoxical sleep (PS) the peak reappears with a latency and amplitude comparable to the response evoked during hyperalertness. Enhanced responses similar to the evoked potentials during PS are seen following treatment with amphetamine, LSD-25 and reserpine, all of which induce an aroused EEG. Reserpine also fosters PS behavior. A group of central depressant drugs including pentobarbital, morphine, chlorpromazine and atropine all markedly reduce the amplitude and increase the latency of the evoked response in dosages which prevent the appearance of PS. The conclusion is reached that PS is not a deep stage of sleep. The results suggest, rather, that PS represents a hyperactive condition of the limbic midbrain component of the brainstem reticular system and that the behavioral depression in PS results from an active inhibition of afferent synapses and/or enhanced activity in the descending bulbar inhibitory system.