Major alteration of motor control during rapid eye movements sleep in mice models of sleep disorders.

Alteration of motor control during rapid eye movements (REM) sleep has been extensively described in sleep disorders, in particular in isolated REM sleep behavior disorder (iRBD) and narcolepsy type 1 (NT1). NT1 is caused by the loss of orexin/hypocretin (ORX) neurons. Unlike in iRBD, the RBD comorbid symptoms of NT1 are not associated with alpha-synucleinopathies.

An electrophysiological correlate of sleep in a shark.

Sleep is a prominent physiological state observed across the animal kingdom. Yet, for some animals, our ability to identify sleep can be masked by behaviors otherwise associated with being awake, such as for some sharks that must swim continuously to push oxygenated seawater over their gills to breathe. We know that sleep in buccal pumping sharks with clear rest/activity cycles, such as draughtsboard sharks (Cephaloscyllium isabellum, Bonnaterre, 1788), manifests as a behavioral shutdown, postural relaxation, reduced responsiveness, and a lowered metabolic rate.

Nesting chinstrap penguins accrue large quantities of sleep through seconds-long microsleeps.

Microsleeps, the seconds-long interruptions of wakefulness by eye closure and sleep-related brain activity, are dangerous when driving and might be too short to provide the restorative functions of sleep. If microsleeps do fulfill sleep functions, then animals faced with a continuous need for vigilance might resort to this sleep strategy. We investigated electroencephalographically defined sleep in wild chinstrap penguins, at sea and while nesting in Antarctica, constantly exposed to an egg predator and aggression from other penguins.

Sleep: Hemispheres fight for dominance.

A new study shows that bearded dragons have a peculiar way to coordinate sleep state changes between brain hemispheres. The hemisphere that acts first imposes its activity on the other during their REM sleep-like state.

Wide-spread brain activation and reduced CSF flow during avian REM sleep.

Mammalian sleep has been implicated in maintaining a healthy extracellular environment in the brain. During wakefulness, neuronal activity leads to the accumulation of toxic proteins, which the glymphatic system is thought to clear by flushing cerebral spinal fluid (CSF) through the brain. In mice, this process occurs during non-rapid eye movement (NREM) sleep.

Pupillary behavior during wakefulness, non-REM sleep, and REM sleep in birds is opposite that of mammals.

Mammalian pupils respond to light and dilate with arousal, attention, cognitive workload, and emotions, thus reflecting the state of the brain. Pupil size also varies during sleep, constricting during deep non-REM sleep and dilating slightly during REM sleep. Anecdotal reports suggest that, unlike mammals, birds constrict their pupils during aroused states, such as courtship and aggression, raising the possibility that pupillary behavior also differs between mammals and birds during sleep.

Granule cells in the infrapyramidal blade of the dentate gyrus are activated during paradoxical (REM) sleep hypersomnia but not during wakefulness: a study using TRAP mice.

Study Objectives: Determine whether in the hippocampus and the supramammillary nucleus (SuM) the same neurons are reactivated when mice are exposed 1 week apart to two periods of wakefulness (W-W), paradoxical sleep rebound (PSR-PSR) or a period of W followed by a period of PSR (W-PSR).

Methods: We combined the innovative TRAP2 mice method in which neurons expressing cFos permanently express tdTomato after tamoxifen injection with cFos immunohistochemistry.

Results: We found out that a large number of tdTomato+ and cFos+ cells are localized in the dentate gyrus (DG) after PSR and W while CA1 and CA3 contained both types of neurons only after W.

Is REM sleep a paradoxical state?: Different neurons are activated in the cingulate cortices and the claustrum during wakefulness and paradoxical sleep hypersomnia.

Michel Jouvet proposed in 1959 that REM sleep is a paradoxical state since it was characterized by the association of a cortical activation similar to wakefulness (W) with muscle atonia. Recently, we showed using cFos as a marker of activity that cortical activation during paradoxical sleep (PS) was limited to a few limbic cortical structures in contrast to W during which all cortices were strongly activated. However, we were not able to demonstrate whether the same neurons are activated during PS and W and to rule out that the activation observed was not linked with stress induced by the flowerpot method of PS deprivation.

Evolutionary Origin of Distinct NREM and REM Sleep.

Sleep is mandatory in most animals that have the nervous system and is universally observed in model organisms ranging from the nematodes, zebrafish, to mammals. However, it is unclear whether different sleep states fulfill common functions and are driven by shared mechanisms in these different animal species. Mammals and birds exhibit two obviously distinct states of sleep, i.

Comparative Perspectives that Challenge Brain Warming as the Primary Function of REM Sleep.

Rapid eye movement (REM) sleep is a paradoxical state of wake-like brain activity occurring after non-REM (NREM) sleep in mammals and birds. In mammals, brain cooling during NREM sleep is followed by warming during REM sleep, potentially preparing the brain to perform adaptively upon awakening. If brain warming is the primary function of REM sleep, then it should occur in other animals with similar states.

Slow Waves Promote Sleep-Dependent Plasticity and Functional Recovery after Stroke.

Functional recovery after stroke is associated with a remapping of neural circuits. This reorganization is often associated with low-frequency, high-amplitude oscillations in the peri-infarct zone in both rodents and humans. These oscillations are reminiscent of sleep slow waves (SW) and suggestive of a role for sleep in brain plasticity that occur during stroke recovery; however, direct evidence is missing.

GABA-glutamate supramammillary neurons control theta and gamma oscillations in the dentate gyrus during paradoxical (REM) sleep.

Several studies suggest that neurons from the lateral region of the SuM (SuML) innervating the dorsal dentate gyrus (DG) display a dual GABAergic and glutamatergic transmission and are specifically activated during paradoxical (REM) sleep (PS). The objective of the present study is to characterize the anatomical, neurochemical and electrophysiological properties of the SuML-DG projection neurons and to determine how they control DG oscillations and neuronal activation during PS and other vigilance states. For this purpose, we combine structural connectivity techniques using neurotropic viral vectors (rabies virus, AAV), neurochemical anatomy (immunohistochemistry, in situ hybridization) and imaging (light, electron and confocal microscopy) with in vitro (patch clamp) and in vivo (LFP, EEG) optogenetic and electrophysiological recordings performed in transgenic VGLUT2-cre male mice.

An Implantable, Low-Power Instrumentation for the Long Term Monitoring of the Sleep of Animals under Natural Conditions.

Sleep is a universal and complex state and it is widely agreed that this state is present in every animal species. However, the evolutionary origins of sleep remain ignored or misunderstood, which has led researchers to study, in various species, this common behaviour of all living organisms. Sleep is commonly studied at various levels under laboratory conditions, using tethered devices which record electroencephalographic or electromyographic readings.

Insights into paradoxical (REM) sleep homeostatic regulation in mice using an innovative automated sleep deprivation method.

Identifying the precise neuronal networks activated during paradoxical sleep (PS, also called REM sleep) has been a challenge since its discovery. Similarly, our understanding of the homeostatic mechanisms regulating PS, whether through external modulation by circadian and ultradian drives or via intrinsic homeostatic regulation, is still limited, largely due to interfering factors rendering the investigation difficult. Indeed, none of the studies published so far were able to manipulate PS without significantly altering slow-wave sleep and/or stress level, thus introducing a potential bias in the analyses.

What Is REM Sleep?

For many decades, sleep researchers have sought to determine which species 'have' rapid eye movement (REM) sleep. In doing so, they relied predominantly on a template derived from the expression of REM sleep in the adults of a small number of mammalian species. Here, we argue for a different approach that focuses less on a binary decision about haves and have nots, and more on the diverse expression of REM sleep components over development and across species.

Artificial light at night disturbs the activity and energy allocation of the common toad during the breeding period.

The presence of artificial light at night (ALAN) is currently a global phenomenon. By altering the photoperiod, ALAN may directly affect the physiology and behaviour of many organisms, such as the timing of daily rhythms, hormonal regulation, food intake, metabolism, migration and reproduction. Surprisingly while it is known that ALAN exposure strongly influences health of humans and laboratory animals, studies on wildlife remain scarce.

ONEIROS, a new miniature standalone device for recording sleep electrophysiology, physiology, temperatures and behavior in the lab and field.

Background: Sleep is an inactive state of reduced environmental awareness shared by all animals. When compared to wakefulness, sleep behavior is associated with changes in physiology and brain activity. The nature of these changes varies considerably across species, and therefore is a rich resource for gaining insight into the evolution and functions of sleep.

INTRAMUSCULAR ADMINISTRATION OF KETAMINE-MEDETOMIDINE ASSURES STABLE ANAESTHESIA NEEDED FOR LONG-TERM SURGERY IN THE ARGENTINE TEGU SALVATOR MERIANAE.

  To define a protocol of anesthesia for long-duration invasive surgery in a lizard, eight young adult Argentine tegus ( Salvator merianae) of mean body weight 3.0 kg (interquartile range [IQR] 3.40-2.

Ventromedial medulla inhibitory neuron inactivation induces REM sleep without atonia and REM sleep behavior disorder.

Despite decades of research, there is a persistent debate regarding the localization of GABA/glycine neurons responsible for hyperpolarizing somatic motoneurons during paradoxical (or REM) sleep (PS), resulting in the loss of muscle tone during this sleep state. Combining complementary neuroanatomical approaches in rats, we first show that these inhibitory neurons are localized within the ventromedial medulla (vmM) rather than within the spinal cord. We then demonstrate their functional role in PS expression through local injections of adeno-associated virus carrying specific short-hairpin RNA in order to chronically impair inhibitory neurotransmission from vmM.

Electrophysiological Evidence That the Retrosplenial Cortex Displays a Strong and Specific Activation Phased with Hippocampal Theta during Paradoxical (REM) Sleep.

It is widely accepted that cortical neurons are similarly more activated during waking and paradoxical sleep (PS; aka REM) than during slow-wave sleep (SWS). However, we recently reported using Fos labeling that only a few limbic cortical structures including the retrosplenial cortex (RSC) and anterior cingulate cortex (ACA) contain a large number of neurons activated during PS hypersomnia. Our aim in the present study was to record local field potentials and unit activity from these two structures across all vigilance states in freely moving male rats to determine whether the RSC and the ACA are electrophysiologically specifically active during basal PS episodes.

Genetic inactivation of glutamate neurons in the rat sublaterodorsal tegmental nucleus recapitulates REM sleep behaviour disorder.

SEE SCHENCK AND MAHOWALD DOI101093/AWW329 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Idiopathic REM sleep behaviour disorder is characterized by the enactment of violent dreams during paradoxical (REM) sleep in the absence of normal muscle atonia. Accumulating clinical and experimental data suggest that REM sleep behaviour disorder might be due to the neurodegeneration of glutamate neurons involved in paradoxical sleep and located within the pontine sublaterodorsal tegmental nucleus. The purpose of the present work was thus to functionally determine first, the role of glutamate sublaterodorsal tegmental nucleus neurons in paradoxical sleep and second, whether their genetic inactivation is sufficient for recapitulating REM sleep behaviour disorder in rats.

The supramammillary nucleus and the claustrum activate the cortex during REM sleep.

Evidence in humans suggests that limbic cortices are more active during rapid eye movement (REM or paradoxical) sleep than during waking, a phenomenon fitting with the presence of vivid dreaming during this state. In that context, it seemed essential to determine which populations of cortical neurons are activated during REM sleep. Our aim in the present study is to fill this gap by combining gene expression analysis, functional neuroanatomy, and neurochemical lesions in rats.