Sleep induced by cortical stimulation

Peñaloza-Rojas, J.H.; Elterman, M.; Olmos, N.

doi:10.1016/0014-4886(64)90091-3

Cited by 34 publications

(5 citation statements)

References 11 publications

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“…Peñaloza-Rojas et al (1964) and Clemente (1968) reported that stimulation to the orbital gyrus of the frontal cortex of cats produced EEG synchronization and behavioral sleep, similar to what Sterman and Clemente (1962a,b) had shown with basal forebrain stimulation. The orbital gyrus is located at the ventral aspect of the frontal cortex and is anatomically and functionally linked with the basal forebrain area described earlier.…”

Section: Thalamic Recruiting and Other Forms Of Induced Slow Wavessupporting

confidence: 54%

The Neural Control of Sleep and Waking

2002

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Library of Congress Cataloging-in-Publication Data Siegel, Jerome H., 1932-The neural control of sleep and waking / Jerome Siegel. p. cm. Includes bibliographical references and index. ISBN 0-387-95536-4 (hardcover: alk. paper) ISBN 0-387-95492-9 (softcover: alk. paper) 1. Sleep-Research-History. 2. Sleep-wake cycle-Research-History. I. Title.QP425 . S585 2002 612.8'21-dc21 2002067019 ISBN 0-387-95536-4 (hardcover) Printed on acid-free paper. ISBN 0-387-95492-9 (softcover)

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Section: Thalamic Recruiting and Other Forms Of Induced Slow Wavessupporting

confidence: 54%

The Neural Control of Sleep and Waking

2002

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“…These observations lend further support to the hypothesis that cortical and subcortical structures play a role in sleep–wake functions. Experimentally, cerebral cortex stimulations, even outside the basal forebrain area, can induce sleep behaviour (Penaloza‐Rojas et al . 1964; Sterman and Clemente 1962).…”

Section: Discussionmentioning

confidence: 99%

Evolution of sleep and sleep EEG after hemispheric stroke

Vock

Achermann

Bischof

et al. 2002

Journal of Sleep Research

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SUMMARY The evolution of subjective sleep and sleep electroencephalogram (EEG) after hemispheric stroke have been rarely studied and the relationship of sleep variables to stroke outcome is essentially unknown. We studied 27 patients with first hemispheric ischaemic stroke and no sleep apnoea in the acute (1–8 days), subacute (9–35 days), and chronic phase (5–24 months) after stroke. Clinical assessment included estimated sleep time per 24 h (EST) and Epworth sleepiness score (ESS) before stroke, as well as EST, ESS and clinical outcome after stroke. Sleep EEG data from stroke patients were compared with data from 11 hospitalized controls and published norms. Changes in EST (>2 h, 38% of patients) and ESS (>3 points, 26%) were frequent but correlated poorly with sleep EEG changes. In the chronic phase no significant differences in sleep EEG between controls and patients were found. High sleep efficiency and low wakefulness after sleep onset in the acute phase were associated with a good long‐term outcome. These two sleep EEG variables improved significantly from the acute to the subacute and chronic phase. In conclusion, hemispheric strokes can cause insomnia, hypersomnia or changes in sleep needs but only rarely persisting sleep EEG abnormalities. High sleep EEG continuity in the acute phase of stroke heralds a good clinical outcome.

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“…In awake cats, full behavioral NREM sleep can be induced by direct 5-Hz electrical stimulation of the PFC [31][32][33] , and these observations are quite striking 32 : "When the orbital frontal cortex stimulation was initiated, the animal would stop eating, walk away from the food dish and lie down. If the stimulation was continued for 45 or 50 sec, the animal would go into slow wave sleep and continue to sleep after the stimulation was discontinued.…”

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confidence: 99%

Sleep deprivation triggers somatostatin neurons in prefrontal cortex to initiate nesting and sleep via the preoptic and lateral hypothalamus

Tossell

Soto

et al. 2020

Preprint

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AbstractAnimals undertake specific behaviors before sleep. Little is known about whether these innate behaviors, such as nest building, are actually an intrinsic part of the sleep-inducing circuitry. We found, using activity-tagging genetics, that mouse prefrontal cortex (PFC) somatostatin/GABAergic (SOM/GABA) neurons, which become activated during sleep deprivation, induce nest building when opto-activated. These tagged neurons induce sustained global NREM sleep if their activation is prolonged metabotropically. Sleep-deprivation-tagged PFC SOM/GABA neurons have long-range projections to the lateral preoptic (LPO) and lateral hypothalamus (LH). Local activation of tagged PFC SOM/GABA terminals in LPO and the LH induced nesting and NREM sleep respectively. Our findings provide a circuit link for how the PFC responds to sleep deprivation by coordinating sleep preparatory behavior and subsequent sleep.

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Sleep induced by cortical stimulation

Cited by 34 publications

References 11 publications

The Neural Control of Sleep and Waking

The Neural Control of Sleep and Waking

Evolution of sleep and sleep EEG after hemispheric stroke

Sleep deprivation triggers somatostatin neurons in prefrontal cortex to initiate nesting and sleep via the preoptic and lateral hypothalamus

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