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Sleepers awake A paper published in Nature in April raised the intriguing possibility that optical therapies might be developed to treat neurological disorders. That work, in tissue slices and in C. elegans roundworms, showed that brain cells can be genetically engineered to alter their activity in response to pulses of different colours of light. A follow-up study now shows that behaviour can be modified in a living mammal by similar means. Hypocretin (Hcrt)-producing neurons in the hypothalamus are active during transitions from sleep to waking states. Optical stimulation of mouse Hcrt neurons engineered to respond to light increases the likelihood of transition from sleep to wakefulness, with higher frequencies causing more abrupt awakening. As Hcrt deficiency is linked to narcolepsy, these results may provide insights into sleep disorders. The neural underpinnings of sleep involve interactions between sleep-promoting areas such as the anterior hypothalamus, and arousal systems located in the posterior hypothalamus, the basal forebrain and the brainstem 1 , 2 . Hypocretin 3 (Hcrt, also known as orexin 4 )-producing neurons in the lateral hypothalamus 5 are important for arousal stability 2 , and loss of Hcrt function has been linked to narcolepsy 6 , 7 , 8 , 9 . However, it is unknown whether electrical activity arising from Hcrt neurons is sufficient to drive awakening from sleep states or is simply correlated with it. Here we directly probed the impact of Hcrt neuron activity on sleep state transitions with in vivo neural photostimulation 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , genetically targeting channelrhodopsin-2 to Hcrt cells and using an optical fibre to deliver light deep in the brain, directly into the lateral hypothalamus, of freely moving mice. We found that direct, selective, optogenetic photostimulation of Hcrt neurons increased the probability of transition to wakefulness from either slow wave sleep or rapid eye movement sleep. Notably, photostimulation using 5–30 Hz light pulse trains reduced latency to wakefulness, whereas 1 Hz trains did not. This study establishes a causal relationship between frequency-dependent activity of a genetically defined neural cell type and a specific mammalian behaviour central to clinical conditions and neurobehavioural physiology.

Memory consolidation has been proposed as a function of sleep. However, sleep is a complex phenomenon characterized by several features including duration, intensity, and continuity. Sleep continuity is disrupted in different neurological and psychiatric conditions, many of which are accompanied by memory deficits. This finding has raised the question of whether the continuity of sleep is important for memory consolidation. However, current techniques used in sleep research cannot manipulate a single sleep feature while maintaining the others constant. Here, we introduce the use of optogenetics to investigate the role of sleep continuity in memory consolidation. We optogenetically targeted hypocretin/orexin neurons, which play a key role in arousal processes. We used optogenetics to activate these neurons at different intervals in behaving mice and were able to fragment sleep without affecting its overall amount or intensity. Fragmenting sleep after the learning phase of the novel object recognition (NOR) task significantly decreased the performance of mice on the subsequent day, but memory was unaffected if the average duration of sleep episodes was maintained at 62–73% of normal. These findings demonstrate the use of optogenetic activation of arousal-related nuclei as a way to systematically manipulate a specific feature of sleep. We conclude that regardless of the total amount of sleep or sleep intensity, a minimal unit of uninterrupted sleep is crucial for memory consolidation.

Light influences sleep and alertness either indirectly through a well-characterized circadian pathway or directly through yet poorly understood mechanisms. Melanopsin (Opn4) is a retinal photopigment crucial for conveying nonvisual light information to the brain. Through extensive characterization of sleep and the electrocorticogram (ECoG) in melanopsin-deficient (Opn4(-/-)) mice under various light-dark (LD) schedules, we assessed the role of melanopsin in mediating the effects of light on sleep and ECoG activity. In control mice, a light pulse given during the habitual dark period readily induced sleep, whereas a dark pulse given during the habitual light period induced waking with pronounced theta (7-10 Hz) and gamma (40-70 Hz) activity, the ECoG correlates of alertness. In contrast, light failed to induce sleep in Opn4(-/-) mice, and the dark-pulse-induced increase in theta and gamma activity was delayed. A 24-h recording under a LD 1-hratio1-h schedule revealed that the failure to respond to light in Opn4(-/-) mice was restricted to the subjective dark period. Light induced c-Fos immunoreactivity in the suprachiasmatic nuclei (SCN) and in sleep-active ventrolateral preoptic (VLPO) neurons was importantly reduced in Opn4(-/-) mice, implicating both sleep-regulatory structures in the melanopsin-mediated effects of light. In addition to these acute light effects, Opn4(-/-) mice slept 1 h less during the 12-h light period of a LD 12ratio12 schedule owing to a lengthening of waking bouts. Despite this reduction in sleep time, ECoG delta power, a marker of sleep need, was decreased in Opn4(-/-) mice for most of the (subjective) dark period. Delta power reached after a 6-h sleep deprivation was similarly reduced in Opn4(-/-) mice. In mice, melanopsin's contribution to the direct effects of light on sleep is limited to the dark or active period, suggesting that at this circadian phase, melanopsin compensates for circadian variations in the photo sensitivity of other light-encoding pathways such as rod and cones. Our study, furthermore, demonstrates that lack of melanopsin alters sleep homeostasis. These findings call for a reevaluation of the role of light on mammalian physiology and behavior.

Slow-wave (SW) and rapid eye movement (REM) sleep states are defining features of mammalian sleep. Controlling them is key to unraveling their function and developing therapeutic strategies for sleep disorders. We investigated sleep state manipulation using light in Pogona vitticeps , a lizard exhibiting highly structured, periodic transitions between sleep states. We demonstrate state entrainment using light pulses, overriding the natural sleep state rhythm, and revealing a mechanism for non-invasive modulation of sleep architecture. External light pulses transiently increase spiking followed by a transition to a SW-like state, characterized by elevated δ/β oscillation power, increased sharp-wave activity, and reduced baseline spiking. This state persists after stimulation offset, and is followed by REM-like activity. Notably, state modulation was wavelength-dependent: white and red lights produced robust entrainment whereas blue and green lights yielded weaker modulation. Replacing external illumination with direct intracranial light delivered via an optic fiber, at intensities commonly used in optogenetics, resulted in similar entrainment and wavelength-dependence, but perturbed natural sleep, as indicated by increased movement and reduced δ/β power. Our findings identify light pulses as a potent strategy for controlling sleep-state dynamics and dissecting the mechanisms and evolutionary origins of sleep-state transitions and their modulation by external light. External and internal (via optic fiber) light pulses modulate lizard sleep states in a wavelength-dependent manner, enabling control of sleep states and highlighting potential indirect effects in optogenetic experiments.

•First investigation of 5 G RF-EMF effects on NREM sleep spindles in genetic context.•Variant rs7304986 of CACNA1C modulates 5 G effects on spindle center frequency.•Exposure to 3.6 GHz 5 G RF-EMF accelerates spindle frequency in T/C allele carriers.•Spindle frequency in T/C carriers accelerated over widespread cortical areas.•Studies elucidating biological mechanisms underlying 5 G RF-EMF effects warranted. The introduction of 5G technology as the latest standard in mobile telecommunications has raised concerns about its potential health effects. Prior studies of earlier generations of radiofrequency electromagnetic fields (RF-EMF) demonstrated narrowband spectral increases in the electroencephalographic (EEG) spindle frequency range (11–16 Hz) in non-rapid-eye-movement (NREM) sleep. However, the impact of 5G RF-EMF on sleep remains unexplored. Additionally, RF-EMF can activate l-type voltage-gated calcium channels (LTCC), which have been linked to sleep quality and EEG oscillatory activity. This study investigates whether the allelic variant rs7304986 in the CACNA1C gene, encoding the α1C subunit of LTCC, modulates 5G RF-EMF effects on EEG spindle activity in NREM sleep. Thirty-four participants, genotyped for rs7304986 (15 T/C and 19 matched T/T carriers), underwent a double-blind, sham-controlled study with standardized left-hemisphere exposure to two 5G RF-EMF signals (3.6 GHz and 700 MHz) for 30 min before sleep. Sleep spindle activity was analyzed using high-density EEG and the Fitting Oscillations & One Over f (FOOOF) algorithm. T/C carriers reported longer sleep latency compared to T/T carriers. A significant interaction between RF-EMF exposure and rs7304986 genotype was observed, with only 3.6 GHz exposure in T/C carriers inducing a faster spindle center frequency in the central, parietal, and occipital cortex compared to sham. These findings suggest that 3.6 GHz 5G RF-EMF modulates spindle center frequency in NREM sleep in a CACNA1C genotype-dependent manner, implicating LTCC in the physiological response to RF-EMF and underscoring the need for further research into 5G effects on brain health.

Light regulates daily sleep rhythms by a neural circuit that connects intrinsically photosensitive retinal ganglion cells (ipRGCs) to the circadian pacemaker, the suprachiasmatic nucleus. Light, however, also acutely affects sleep in a circadian-independent manner. The neural circuits involving the acute effect of light on sleep remain unknown. Here we uncovered a neural circuit that drives this acute light response, independent of the suprachiasmatic nucleus, but still through ipRGCs. We show that ipRGCs substantially innervate the preoptic area (POA) to mediate the acute light effect on sleep in mice. Consistently, activation of either the POA projecting ipRGCs or the light-responsive POA neurons increased non-rapid eye movement (NREM) sleep without influencing REM sleep. In addition, inhibition of the light-responsive POA neurons blocked the acute light effects on NREM sleep. The predominant light-responsive POA neurons that receive ipRGC input belong to the corticotropin-releasing hormone subpopulation. Remarkably, the light-responsive POA neurons are inhibitory and project to well-known wakefulness-promoting brain regions, such as the tuberomammillary nucleus and the lateral hypothalamus. Therefore, activation of the ipRGC-POA circuit inhibits arousal brain regions to drive light-induced NREM sleep. Our findings reveal a functional retina-brain circuit that is both necessary and sufficient for the acute effect of light on sleep. The preoptic area (POA) is critical for sleep regulation but its role in acute, non-circadian, light effects on sleep are unclear. The authors show that intrinsically photosensitive retinal ganglion cells provide substantial input into the POA and through these modulate the amount of non-rapid eye movement (NREM) sleep.

The effects of ionizing radiation (cobalt-60 γ-ray) on the central nervous system were studied by electroencephalography on unrestrained and nonanesthetized adult rabbits with permanent electrodes implanted into the cortical area and several subcortical regions. The changes in threshold value of EEG afterreaction (EA) induced by low-frequency square waves, as well as the changes in the appearance of spontaneous EA, were examined, and the following results were obtained. 1. A single exposure of 20 or 50 R to the whole head resulted in a transient elevation in threshold value for 3 to 9 hours, irrespective of the dose given. 2. After an exposure of 100 R or more there was an almost linear relationship between the maximum threshold value and the given exposure, but the individual difference was noticeable at 100 R or less. 3. Dose dependency was observed in the time for the elevated threshold value to recover completely. 4. A transient disappearance and decrease in appearance time were observed in the spontaneous EA at exposures above 500 R, and a relative increase of the ratio of EEG spindle-burst stage to EA at exposures above 1000 R.

Understanding the non-visual effects of light is increasingly important, as circadian disruption from inappropriate exposure negatively impacts sleep, metabolism, and cognition. However, artificial lighting is rarely designed from a non-visual illuminance perspective, and its effects on biological rhythms remain incompletely evaluated. Here, we investigated three lighting conditions in rats: conventional light–dark (L/D), and two novel settings with matched visual illuminance but differing nighttime rat melanopic equivalent daylight illuminance (2–4 lx; rat mel EDI), enabled by tunable four-package white light-emitting diodes. Circadian rhythms were assessed using physiological (core body temperature, heart rate, locomotor activity) and neurophysiological markers (non-rapid eye movement sleep index, θ–γ cross-frequency coupling) across rhythmicity (periodicity, amplitude), stability (inter-daily stability, intra-daily variability), and state classification (Gaussian mixture modeling, k-means clustering). Relative to 4 lx, the 2 lx lighting most closely resembled L/D in minimizing rhythm loss and maintaining sleep–wake synchrony. Furthermore, after circadian disruption, switching to the 2 lx lighting restored physiological and neurophysiological markers. These findings indicate that spectrally optimized 2 lx lighting is a viable strategy to maintain or reinstate circadian health when nighttime illumination is unavoidable.

Far-infrared (FIR)-emitting textiles are increasingly used in sleepwear; however, their influence on sleep physiology has not been comprehensively evaluated with multi-modal wearable sensing. This randomized, double-blind, placebo-controlled crossover study examined whether FIR-emitting garments modulate nocturnal thermoregulation, autonomic activity, and sleep architecture. Fifteen healthy young men completed two overnight laboratory sleep sessions wearing either FIR-emitting garments or visually matched polyester controls. Tympanic membrane temperature (TMT), sweating rate, skin temperature, and humidity were continuously monitored using wearable sensors, and sleep stages and heart rate variability (HRV) were assessed using validated portable systems. Compared with control garments, FIR garments produced consistently lower TMT across the night (p = 0.004) and reduced mid-sleep sweating (condition × time interaction: p = 0.026). The proportion of rapid eye movement (REM) sleep was higher in the FIR condition (22.2% ± 6.5% vs. 18.6% ± 6.5%, p = 0.027), despite no changes in total sleep time or sleep efficiency. A transient increase in low-frequency power during early sleep (p = 0.027) suggested baroreflex-related thermal adjustments without sympathetic activation. These findings indicate that FIR-emitting garments facilitate mild nocturnal heat dissipation and support REM expression, demonstrating their potential as a passive intervention to improve sleep-related thermal environments.

The basal forebrain (BF) plays a crucial role in cortical activation. Our previous study showed that activation of cholinergic BF neurons alone is sufficient to suppress slow-wave sleep (SWS) and promote wakefulness and rapid-eye-movement (REM) sleep. However, the exact role of silencing cholinergic BF neurons in the sleep-wake cycle remains unclear. We inhibitied the cholinergic BF neurons genetically targeted with archaerhodopsin (Arch) with yellow light to clarify the role of cholinergic BF neurons in the sleep-wake cycle. Bilateral inactivation of cholinergic BF neurons genetically targeted with archaerhodopsin prolonged SWS and decreased the probability of awakening from SWS in mice. However, silencing these neurons changed neither the duration of wakefulness or REM sleep, nor the probability of transitions to other sleep-wake episodes from wakefulness or REM sleep. Furthermore, silencing these neurons for 6 h within the inactive or active period increased the duration of SWS at the expense of the duration of wakefulness, as well as increasing the number of prolonged SWS episodes (120-240 s). The lost wakefulness was compensated by a delayed increase of wakefulness, so the total duration of SWS and wakefulness during 24 h was kept stable. Our results indicate that the main effect of these neurons is to terminate SWS, whereas wakefulness or REM sleep may be determined by co-operation of the cholinergic BF neurons with other arousal-sleep control systems.