REM sleep: Out-dreaming fear.

The ability to forget fear-inducing situations is essential for adapting to our environment, but the neural mechanisms underlying 'fear forgetting' remain unclear. Novel findings reveal that the activity of the infralimbic cortex - specifically during REM sleep - contributes to the extinction of fear memory.

Sleep: How stress keeps you up at night.

Stress disrupts sleep, but the neural mechanisms underlying this relationship remain unclear. Novel findings in mice reveal a hypothalamic circuit that fragments sleep and promotes arousal after stress.

Immortal orexin cell transplants restore motor-arousal synchrony during cataplexy.

Waking behaviors such as sitting or standing require suitable levels of muscle tone. But it is unclear how arousal and motor circuits communicate with one another so that appropriate motor tone occurs during wakefulness. Cataplexy is a peculiar condition in which muscle tone is involuntarily lost during normal periods of wakefulness.

A novel machine learning system for identifying sleep-wake states in mice.

Research into sleep-wake behaviors relies on scoring sleep states, normally done by manual inspection of electroencephalogram (EEG) and electromyogram (EMG) recordings. This is a highly time-consuming process prone to inter-rater variability. When studying relationships between sleep and motor function, analyzing arousal states under a four-state system of active wake (AW), quiet wake (QW), nonrapid-eye-movement (NREM) sleep, and rapid-eye-movement (REM) sleep provides greater precision in behavioral analysis but is a more complex model for classification than the traditional three-state identification (wake, NREM, and REM sleep) usually used in rodent models.

Neuroscience: Glutamate neurons in the medial septum control wakefulness.

Despite intensive research efforts, biologists still do not have a clear picture of the brain circuitry that controls behavioural arousal. However, new research has identified a novel septo-hypothalamic circuit that functions to promote wakefulness.

The Sublaterodorsal Tegmental Nucleus Functions to Couple Brain State and Motor Activity during REM Sleep and Wakefulness.

Appropriate levels of muscle tone are needed to support waking behaviors such as sitting or standing. However, it is unclear how the brain functions to couple muscle tone with waking behaviors. Cataplexy is a unique experiment of nature in which muscle paralysis involuntarily intrudes into otherwise normal periods of wakefulness.

Newly identified sleep-wake and circadian circuits as potential therapeutic targets.

Optogenetics and chemogenetics are powerful tools, allowing the specific activation or inhibition of targeted neuronal subpopulations. Application of these techniques to sleep and circadian research has resulted in the unveiling of several neuronal populations that are involved in sleep-wake control, and allowed a comprehensive interrogation of the circuitry through which these nodes are coordinated to orchestrate the sleep-wake cycle. In this review, we discuss six recently described sleep-wake and circadian circuits that show promise as therapeutic targets for sleep medicine.

Activation of the Hypoglossal to Tongue Musculature Motor Pathway by Remote Control.

Reduced tongue muscle tone precipitates obstructive sleep apnea (OSA), and activation of the tongue musculature can lessen OSA. The hypoglossal motor nucleus (HMN) innervates the tongue muscles but there is no pharmacological agent currently able to selectively manipulate a channel (e.g.

GABA Cells in the Central Nucleus of the Amygdala Promote Cataplexy.

Cataplexy is a hallmark of narcolepsy characterized by the sudden uncontrollable onset of muscle weakness or paralysis during wakefulness. It can occur spontaneously, but is typically triggered by positive emotions such as laughter. Although cataplexy was identified >130 years ago, its neural mechanism remains unclear.

REM Sleep at its Core - Circuits, Neurotransmitters, and Pathophysiology.

Rapid eye movement (REM) sleep is generated and maintained by the interaction of a variety of neurotransmitter systems in the brainstem, forebrain, and hypothalamus. Within these circuits lies a core region that is active during REM sleep, known as the subcoeruleus nucleus (SubC) or sublaterodorsal nucleus. It is hypothesized that glutamatergic SubC neurons regulate REM sleep and its defining features such as muscle paralysis and cortical activation.

Mechanisms of REM sleep in health and disease.

Purpose Of Review: Our understanding of rapid eye movement (REM) sleep and how it is generated remains a topic of debate. Understanding REM sleep mechanisms is important because several sleep disorders result from disturbances in the neural circuits that control REM sleep and its characteristics. This review highlights recent work concerning how the central nervous system regulates REM sleep, and how the make up and breakdown of these REM sleep-generating circuits contribute to narcolepsy, REM sleep behaviour disorder and sleep apnea.

Brain biology: jerked around by sleep.

During rapid eye movement sleep, the forelimb muscles of newborn rats jerk and twitch in an organized pattern, the fidelity of which improves with time. The coordinated nature of such sleep movements may instruct the developing brain how to more effectively execute movements during wakefulness.

Sleep biology: tuning in while tuned out.

The barrel cortex and whisker thalamus preferentially respond to whisker movements during REM sleep in infant rats. Understanding why the brain tunes into sensory signals while it's tuned out in sleep may provide clues about the functions of REM sleep.

Tonic and phasic drive to medullary respiratory neurons during periodic breathing.

It is unknown how central neural activity produces the repetitive termination and restart of periodic breathing (PB). We hypothesized that inspiratory and expiratory neural activities would be greatest during the waxing phase and least during the waning phase. We analyzed diaphragmatic and medullary respiratory neural activities during PB in intact unanesthetized adult cats.

Phasic motor activity of respiratory and non-respiratory muscles in REM sleep.

Objectives: In this study, we quantified the profiles of phasic activity in respiratory muscles (diaphragm, genioglossus and external intercostal) and non-respiratory muscles (neck and extensor digitorum) across REM sleep. We hypothesized that if there is a unique pontine structure that controls all REM sleep phasic events, the profiles of the phasic twitches of different muscle groups should be identical. Furthermore, we described how respiratory parameters (e.

Effect of hypercapnia on sleep and breathing in unanesthetized cats.

Objectives: In this study, we looked at the effect of hypercapnia on sleep architecture and breathing. We characterized the effect of hypercapnia on duration, frequency, and latency of NREM and REM sleep. We described state-specific patterns of breathing as well.

Medullary respiratory neural activity during hypoxia in NREM and REM sleep in the cat.

Intact unanesthetized cats hyperventilate in response to hypocapnic hypoxia in both wakefulness and sleep. This hyperventilation is caused by increases in diaphragmatic activity during inspiration and expiration. In this study, we recorded 120 medullary respiratory neurons during sleep in hypoxia.

Hypocapnia decreases the amount of rapid eye movement sleep in cats.

Context: Sleep is disturbed at high altitudes. Low PO2 levels at high altitude cause hyperventilation, which results in secondary hypocapnia (low PaCO2 levels). Thus, although sleep disruption at high altitudes is generally assumed to be caused by hypoxia, it may instead be the result of hypocapnia.