Sleep and Thermoregulation in Birds: Cold Exposure Reduces Brain Temperature but Has Little Influence on Sleep Time and Sleep Architecture in Jackdaws (Coloeus monedula).

Birds have an electrophysiological sleep state that resembles mammalian rapid-eye-movement (REM) sleep. However, whether its regulation and function are similar is unclear. In the current experiment, we studied REM sleep regulation in jackdaws (Coloeus monedula) by exposing the birds to low ambient temperature, a procedure that selectively suppresses REM sleep in mammals. Eight jackdaws were equipped with electrodes to record brain activity and neck muscle activity and a thermistor to record cortical brain temperature. Recordings covered a three-day period starting with a 24 h baseline day at an ambient temperature of 21 °C, followed by a 12 h cold night at 4 °C, after which the ambient temperature was restored to 21 °C for the remaining recovery period. Cold exposure at night caused a significant drop in brain temperature of 1.4 °C compared to the baseline night. However, throughout the cold night, jackdaws expressed NREM sleep and REM sleep levels that were not significantly different from the baseline. Also, EEG spectral power during NREM sleep was unaffected by cold exposure. Thus, while cold exposure had a clear effect on brain temperature in jackdaws, it did not have the same REM sleep suppressing effect reported for mammals. These findings suggest that the REM-sleep-like state in birds, unlike REM sleep in mammals, is protected against the influence of low temperature.

A prefrontal-thalamic circuit encodes social information for social recognition.

Social recognition encompasses encoding social information and distinguishing unfamiliar from familiar individuals to form social relationships. Although the medial prefrontal cortex (mPFC) is known to play a role in social behavior, how identity information is processed and by which route it is communicated in the brain remains unclear. Here we report that a ventral midline thalamic area, nucleus reuniens (Re) that has reciprocal connections with the mPFC, is critical for social recognition in male mice. In vivo single-unit recordings and decoding analysis reveal that neural populations in both mPFC and Re represent different social stimuli, however, mPFC coding capacity is stronger. We demonstrate that chemogenetic inhibitions of Re impair the mPFC-Re neural synchronization and the mPFC social coding. Projection pathway-specific inhibitions by optogenetics reveal that the reciprocal connectivity between the mPFC and the Re is necessary for social recognition. These results reveal an mPFC-thalamic circuit for social information processing.

Semelparous marsupials reduce sleep for sex.

Sleep is a prominent, seemingly universal animal behavior. Although sleep maintains optimal waking performance, the biological drive to sleep may be incompatible with the life history of some species. In a multi-year study on semelparous marsupials in Australia, we provide the first direct evidence of ecological sleep restriction in a terrestrial mammal. Dusky (Antechinus swainsonii) and agile (A. agilis) antechinus have an unusual reproductive strategy characterized by the synchronous death of all males at the end of their only breeding season. Using accelerometry, electrophysiology, and metabolomics, we show that males, but not females, increase their activity during the breeding season by reducing sleep. In a trade-off between the neurophysiological requirements for sleep and evolutionary necessity for reproduction, strong sexual selection might drive males to sacrifice sleep to increase access to fertile females and ultimately maximize their fitness.

Neurophysiological and behavioral synchronization in group-living and sleeping mice.

Social interactions profoundly influence animal development, physiology, and behavior. Yet, how sleep-a central behavioral and neurophysiological process-is modulated by social interactions is poorly understood. Here, we characterized sleep behavior and neurophysiology in freely moving and co-living mice under different social conditions. We utilized wireless neurophysiological devices to simultaneously record multiple individuals within a group for 24 h, alongside video acquisition. We first demonstrated that mice seek physical contact before sleep initiation and sleep while in close proximity to each other (hereafter, "huddling"). To determine whether huddling during sleep is a motivated behavior, we devised a novel behavioral apparatus allowing mice to choose whether to sleep in close proximity to a conspecific or in solitude, under different environmental conditions. We also applied a deep-learning-based approach to classify huddling behavior. We demonstrate that mice are willing to forgo their preferred sleep location, even under thermoneutral conditions, to gain access to social contact during sleep. This strongly suggests that the motivation for prolonged physical contact-which we term somatolonging-drives huddling behavior. We then characterized sleep architecture under different social conditions and uncovered a social-dependent modulation of sleep. We also revealed coordination in multiple neurophysiological features among co-sleeping individuals, including in the timing of falling asleep and waking up and non-rapid eye movement sleep (NREMS) intensity. Notably, the timing of rapid eye movement sleep (REMS) was synchronized among co-sleeping male siblings but not co-sleeping female or unfamiliar mice. Our findings provide novel insights into the motivation for physical contact and the extent of social-dependent plasticity in sleep.

Seasonal variation in sleep time: jackdaws sleep when it is dark, but do they really need it?

Sleep is an important behavioural and physiological state that is ubiquitous throughout the animal kingdom. Birds are an interesting group to study sleep since they share similar sleep features with mammals. Interestingly, sleep time in birds has been shown to vary greatly amongst seasons. To understand the mechanisms behind these variations in sleep time, we did an electro-encephalogram (EEG) study in eight European jackdaws (Coloeus monedula) in winter and summer under outdoor seminatural conditions. To assess whether the amount and pattern of sleep is determined by the outdoor seasonal state of the animals or directly determined by the indoor light-dark cycle, we individually housed them indoors where we manipulated the light-dark (LD) cycles to mimic long winter nights (8:16 LD) and short summer nights (16:8 LD) within both seasons. Jackdaws showed under seminatural outdoor conditions 5 h less sleep in summer compared to winter. During the indoor conditions, the birds rapidly adjusted their sleep time to the new LD cycle. Although they swiftly increased or decreased their sleep time, sleep intensity did not vary. The results indicate that the strong seasonal differences in sleep time are largely and directly driven by the available dark time, rather than an endogenous annual clock. Importantly, these findings confirm that sleep in birds is not a rigid phenomenon but highly sensitive to environmental factors.

Somatostatin neurons in prefrontal cortex initiate sleep-preparatory behavior and sleep via the preoptic and lateral hypothalamus.

The prefrontal cortex (PFC) enables mammals to respond to situations, including internal states, with appropriate actions. One such internal state could be 'tiredness'. Here, using activity tagging in the mouse PFC, we identified particularly excitable, fast-spiking, somatostatin-expressing, γ-aminobutyric acid (GABA) (PFCSst-GABA) cells that responded to sleep deprivation. These cells projected to the lateral preoptic (LPO) hypothalamus and the lateral hypothalamus (LH). Stimulating PFCSst-GABA terminals in the LPO hypothalamus caused sleep-preparatory behavior (nesting, elevated theta power and elevated temperature), and stimulating PFCSst-GABA terminals in the LH mimicked recovery sleep (non-rapid eye-movement sleep with higher delta power and lower body temperature). PFCSst-GABA terminals had enhanced activity during nesting and sleep, inducing inhibitory postsynaptic currents on diverse cells in the LPO hypothalamus and the LH. The PFC also might feature in deciding sleep location in the absence of excessive fatigue. These findings suggest that the PFC instructs the hypothalamus to ensure that optimal sleep takes place in a suitable place.

Brain activity of diving seals reveals short sleep cycles at depth.

Sleep is a crucial part of the daily activity patterns of mammals. However, in marine species that spend months or entire lifetimes at sea, the location, timing, and duration of sleep may be constrained. To understand how marine mammals satisfy their daily sleep requirements while at sea, we monitored electroencephalographic activity in wild northern elephant seals (Mirounga angustirostris) diving in Monterey Bay, California. Brain-wave patterns showed that seals took short (less than 20 minutes) naps while diving (maximum depth 377 meters; 104 sleeping dives). Linking these patterns to accelerometry and the time-depth profiles of 334 free-ranging seals (514,406 sleeping dives) revealed a North Pacific sleepscape in which seals averaged only 2 hours of sleep per day for 7 months, rivaling the record for the least sleep among all mammals, which is currently held by the African elephant (about 2 hours per day).

NMDA Receptors in the Lateral Preoptic Hypothalamus Are Essential for Sustaining NREM and REM Sleep.

The lateral preoptic (LPO) hypothalamus is a center for NREM and REM sleep induction and NREM sleep homeostasis. Although LPO is needed for NREM sleep, we found that calcium signals were, surprisingly, highest in REM sleep. Furthermore, and equally surprising, NMDA receptors in LPO were the main drivers of excitation. Deleting the NMDA receptor GluN1 subunit from LPO abolished calcium signals in all cells and produced insomnia. Mice of both sexes had highly fragmented NREM sleep-wake patterns and could not generate conventionally classified REM sleep. The sleep phenotype produced by deleting NMDA receptors depended on where in the hypothalamus the receptors were deleted. Deleting receptors from the anterior hypothalamic area (AHA) did not influence sleep-wake states. The sleep fragmentation originated from NMDA receptors on GABA neurons in LPO. Sleep fragmentation could be transiently overcome with sleeping medication (zolpidem) or sedatives (dexmedetomidine; Dex). By contrast, fragmentation persisted under high sleep pressure produced by sleep deprivation (SD), mice had a high propensity to sleep but woke up. By analyzing changes in δ power, sleep homeostasis (also referred to as "sleep drive") remained intact after NMDA receptor ablation. We suggest NMDA glutamate receptor activation stabilizes firing of sleep-on neurons and that mechanisms of sleep maintenance differ from that of the sleep drive itself.SIGNIFICANCE STATEMENT Insomnia is a common affliction. Most insomniacs feel that they do not get enough sleep, but in fact, often have good amounts of sleep. Their sleep, however, is fragmented, and sufferers wake up feeling unrefreshed. It is unknown how sleep is maintained once initiated. We find that in mice, NMDA-type glutamate receptors in the hypothalamus are the main drivers of excitation and are required for a range of sleep properties: they are, in fact, needed for both sustained NREM sleep periods, and REM sleep generation. When NMDA receptors are selectively reduced from inhibitory preoptic (PO) neurons, mice have normal total amounts of sleep but high sleep-wake fragmentation, providing a model for studying intractable insomnia.

A specific circuit in the midbrain detects stress and induces restorative sleep.

In mice, social defeat stress (SDS), an ethological model for psychosocial stress, induces sleep. Such sleep could enable resilience, but how stress promotes sleep is unclear. Activity-dependent tagging revealed a subset of ventral tegmental area γ-aminobutyric acid (GABA)-somatostatin (VTAVgat-Sst) cells that sense stress and drive non-rapid eye movement (NREM) and REM sleep through the lateral hypothalamus and also inhibit corticotropin-releasing factor (CRF) release in the paraventricular hypothalamus. Transient stress enhances the activity of VTAVgat-Sst cells for several hours, allowing them to exert their sleep effects persistently. Lesioning of VTAVgat-Sst cells abolished SDS-induced sleep; without it, anxiety and corticosterone concentrations remained increased after stress. Thus, a specific circuit allows animals to restore mental and body functions by sleeping, potentially providing a refined route for treating anxiety disorders.

Sleep architecture and regulation of male dusky antechinus, an Australian marsupial.

STUDY OBJECTIVES: In this study, we (1) describe sleep behavior and architecture, and (2) explore how sleep is regulated in dusky antechinus (Antechinus swainsonii), a small insectivorous marsupial. Our aim is to provide the first investigation into sleep homeostasis in a marsupial. METHODS: Wild-caught male dusky antechinus (n = 4) were individually housed in large indoor cages under a natural photoperiod of 10.5 h light/13.5 h dark. Continuous recordings of EEG, EMG, and tri-axial accelerometry were performed under baseline conditions and following 4-h of extended wakefulness. RESULTS: Antechinus engage in SWS and REM sleep. Some aspects of these states are mammal-like, including a high amount (23%) of REM sleep, but other features are reminiscent of birds, notably, hundreds of short sleep episodes (SWS mean: 34 s; REM sleep: 10 s). Antechinus are cathemeral and sleep equally during the night and day. Immediately after the sleep deprivation ended, the animals engaged in more SWS, longer SWS episodes, and greater SWS SWA. The animals did not recover lost REM sleep. CONCLUSIONS: Sleep architecture in dusky antechinus was broadly similar to that observed in eutherian and marsupial mammals, but with interesting peculiarities. We also provided the first evidence of SWS homeostasis in a marsupial mammal.

Sleep loss impairs cognitive performance and alters song output in Australian magpies.

Sleep maintains optimal brain functioning to facilitate behavioural flexibility while awake. Owing to a historical bias towards research on mammals, we know comparatively little about the role of sleep in facilitating the cognitive abilities of birds. We investigated how sleep deprivation over the full-night (12 h) or half-night (6 h) affects cognitive performance in adult Australian magpies (Cracticus tibicen), relative to that after a night of undisturbed sleep. Each condition was preceded and followed by a baseline and recovery night of sleep, respectively. Prior to each treatment, birds were trained on an associative learning task; on the day after experimental treatment (recovery day), birds were tested on a reversal learning task. To glean whether sleep loss affected song output, we also conducted impromptu song recordings for three days. Ultimately, sleep-deprived magpies were slower to attempt the reversal learning task, less likely to perform and complete the task, and those that did the test performed worse than better-rested birds. We also found that sleep-deprived magpies sang longer yet fewer songs, shifted crepuscular singing to mid-day, and during the post-recovery day, song frequency bandwidth narrowed. These results collectively indicate that sleep loss impairs motivation and cognitive performance, and alters song output, in a social adult songbird.

Homeostatic regulation of NREM sleep, but not REM sleep, in Australian magpies.

STUDY OBJECTIVES: We explore non-rapid eye movement (NREM) and rapid eye movement (REM) sleep homeostasis in Australian magpies (Cracticus tibicen tyrannica). We predicted that magpies would recover lost sleep by spending more time in NREM and REM sleep, and by engaging in more intense NREM sleep as indicated by increased slow-wave activity (SWA). METHODS: Continuous 72-h recordings of EEG, EMG, and tri-axial accelerometry, along with EEG spectral analyses, were performed on wild-caught Australian magpies housed in indoor aviaries. Australian magpies were subjected to two protocols of night-time sleep deprivation: full 12-h night (n = 8) and first 6-h half of the night (n = 5), which were preceded by a 36-h baseline recording and followed by a 24-h recovery period. RESULTS: Australian magpies recovered from lost NREM sleep by sleeping more, with increased NREM sleep consolidation, and increased SWA during recovery sleep. Following 12-h of night-time sleep loss, magpies also showed reduced SWA the following night after napping more during the recovery day. Surprisingly, the magpies did not recover any lost REM sleep. CONCLUSIONS: Only NREM sleep is homeostatically regulated in Australian magpies with the level of SWA reflecting prior sleep/wake history. The significance of emerging patterns on the apparent absence of REM sleep homeostasis, now observed in multiple species, remains unclear.

Nitric Oxide Synthase Neurons in the Preoptic Hypothalamus Are NREM and REM Sleep-Active and Lower Body Temperature.

When mice are exposed to external warmth, nitric oxide synthase (NOS1) neurons in the median and medial preoptic (MnPO/MPO) hypothalamus induce sleep and concomitant body cooling. However, how these neurons regulate baseline sleep and body temperature is unknown. Using calcium photometry, we show that NOS1 neurons in MnPO/MPO are predominantly NREM and REM active, especially at the boundary of wake to NREM transitions, and in the later parts of REM bouts, with lower activity during wakefulness. In addition to releasing nitric oxide, NOS1 neurons in MnPO/MPO can release GABA, glutamate and peptides. We expressed tetanus-toxin light-chain in MnPO/MPO NOS1 cells to reduce vesicular release of transmitters. This induced changes in sleep structure: over 24 h, mice had less NREM sleep in their dark (active) phase, and more NREM sleep in their light (sleep) phase. REM sleep episodes in the dark phase were longer, and there were fewer REM transitions between other vigilance states. REM sleep had less theta power. Mice with synaptically blocked MnPO/MPO NOS1 neurons were also warmer than control mice at the dark-light transition (ZT0), as well as during the dark phase siesta (ZT16-20), where there is usually a body temperature dip. Also, at this siesta point of cooled body temperature, mice usually have more NREM, but mice with synaptically blocked MnPO/MPO NOS1 cells showed reduced NREM sleep at this time. Overall, MnPO/MPO NOS1 neurons promote both NREM and REM sleep and contribute to chronically lowering body temperature, particularly at transitions where the mice normally enter NREM sleep.

Hidden Markov models identify major movement modes in accelerometer and magnetometer data from four albatross species.

BACKGROUND: Inertial measurement units (IMUs) with high-resolution sensors such as accelerometers are now used extensively to study fine-scale behavior in a wide range of marine and terrestrial animals. Robust and practical methods are required for the computationally-demanding analysis of the resulting large datasets, particularly for automating classification routines that construct behavioral time series and time-activity budgets. Magnetometers are used increasingly to study behavior, but it is not clear how these sensors contribute to the accuracy of behavioral classification methods. Development of effective  classification methodology is key to understanding energetic and life-history implications of foraging and other behaviors. METHODS: We deployed accelerometers and magnetometers on four species of free-ranging albatrosses and evaluated the ability of unsupervised hidden Markov models (HMMs) to identify three major modalities in their behavior: 'flapping flight', 'soaring flight', and 'on-water'. The relative contribution of each sensor to classification accuracy was measured by comparing HMM-inferred states with expert classifications identified from stereotypic patterns observed in sensor data. RESULTS: HMMs provided a flexible and easily interpretable means of classifying behavior from sensor data. Model accuracy was high overall (92%), but varied across behavioral states (87.6, 93.1 and 91.7% for 'flapping flight', 'soaring flight' and 'on-water', respectively). Models built on accelerometer data alone were as accurate as those that also included magnetometer data; however, the latter were useful for investigating slow and periodic behaviors such as dynamic soaring at a fine scale. CONCLUSIONS: The use of IMUs in behavioral studies produces large data sets, necessitating the development of computationally-efficient methods to automate behavioral classification in order to synthesize and interpret underlying patterns. HMMs provide an accessible and robust framework for analyzing complex IMU datasets and comparing behavioral variation among taxa across habitats, time and space.

Cloud cover amplifies the sleep-suppressing effect of artificial light at night in geese.

In modern society the night sky is lit up not only by the moon but also by artificial light devices. Both of these light sources can have a major impact on wildlife physiology and behaviour. For example, a number of bird species were found to sleep several hours less under full moon compared to new moon and a similar sleep-suppressing effect has been reported for artificial light at night (ALAN). Cloud cover at night can modulate the light levels perceived by wildlife, yet, in opposite directions for ALAN and moon. While clouds will block moon light, it may reflect and amplify ALAN levels and increases the night glow in urbanized areas. As a consequence, cloud cover may also modulate the sleep-suppressing effects of moon and ALAN in different directions. In this study we therefore measured sleep in barnacle geese (Branta leucopsis) under semi-natural conditions in relation to moon phase, ALAN and cloud cover. Our analysis shows that, during new moon nights stronger cloud cover was indeed associated with increased ALAN levels at our study site. In contrast, light levels during full moon nights were fairly constant, presumably because of moonlight on clear nights or because of reflected artificial light on cloudy nights. Importantly, cloud cover caused an estimated 24.8% reduction in the amount of night-time NREM sleep from nights with medium to full cloud cover, particularly during new moon when sleep was unaffected by moon light. In conclusion, our findings suggest that cloud cover can, in a rather dramatic way, amplify the immediate effects of ALAN on wildlife. Sleep appears to be highly sensitive to ALAN and may therefore be a good indicator of its biological effects.

Characterization of exploratory patterns and hippocampal-prefrontal network oscillations during the emergence of free exploration.

During free exploration, the emergence of patterned and sequential behavioral responses to an unknown environment reflects exploration traits and adaptation. However, the behavioral dynamics and neural substrates underlying the exploratory behavior remain poorly understood. We developed computational tools to quantify the exploratory behavior and performed in vivo electrophysiological recordings in a large arena in which mice made sequential excursions into unknown territory. Occupancy entropy was calculated to characterize the cumulative and moment-to-moment behavioral dynamics in explored and unexplored territories. Local field potential analysis revealed that the theta activity in the dorsal hippocampus (dHPC) was highly correlated with the occupancy entropy. Individual dHPC and prefrontal cortex (PFC) oscillatory activities could classify various aspects of free exploration. Initiation of exploration was accompanied by a coordinated decrease and increase in theta activity in PFC and dHPC, respectively. Our results indicate that dHPC and PFC work synergistically in shaping free exploration by modulating exploratory traits during emergence and visits to an unknown environment.

Dysfunction of ventral tegmental area GABA neurons causes mania-like behavior.

The ventral tegmental area (VTA), an important source of dopamine, regulates goal- and reward-directed and social behaviors, wakefulness, and sleep. Hyperactivation of dopamine neurons generates behavioral pathologies. But any roles of non-dopamine VTA neurons in psychiatric illness have been little explored. Lesioning or chemogenetically inhibiting VTA GABAergic (VTAVgat) neurons generated persistent wakefulness with mania-like qualities: locomotor activity was increased; sensitivity to D-amphetamine was heightened; immobility times decreased on the tail suspension and forced swim tests; and sucrose preference increased. Furthermore, after sleep deprivation, mice with lesioned VTAVgat neurons did not catch up on lost sleep, even though they were starting from a sleep-deprived baseline, suggesting that sleep homeostasis was bypassed. The mania-like behaviors, including the sleep loss, were reversed by valproate, and re-emerged when treatment was stopped. Lithium salts and lamotrigine, however, had no effect. Low doses of diazepam partially reduced the hyperlocomotion and fully recovered the immobility time during tail suspension. The mania like-behaviors mostly depended on dopamine, because giving D1/D2/D3 receptor antagonists reduced these behaviors, but also partially on VTAVgat projections to the lateral hypothalamus (LH). Optically or chemogenetically inhibiting VTAVgat terminals in the LH elevated locomotion and decreased immobility time during the tail suspension and forced swimming tests. VTAVgat neurons help set an animal's (and perhaps human's) mental and physical activity levels. Inputs inhibiting VTAVgat neurons intensify wakefulness (increased activity, enhanced alertness and motivation), qualities useful for acute survival. In the extreme, however, decreased or failed inhibition from VTAVgat neurons produces mania-like qualities (hyperactivity, hedonia, decreased sleep).

Seasonal variation in sleep homeostasis in migratory geese: a rebound of NREM sleep following sleep deprivation in summer but not in winter.

Sleep is a behavioral and physiological state that is thought to serve important functions. Many animals go through phases in the annual cycle where sleep time might be limited, for example, during the migration and breeding phases. This leads to the question whether there are seasonal changes in sleep homeostasis. Using electroencephalogram (EEG) data loggers, we measured sleep in summer and winter in 13 barnacle geese (Branta leucopsis) under semi-natural conditions. During both seasons, we examined the homeostatic regulation of sleep by depriving the birds of sleep for 4 and 8 h after sunset. In winter, barnacle geese showed a clear diurnal rhythm in sleep and wakefulness. In summer, this rhythm was less pronounced, with sleep being spread out over the 24-h cycle. On average, the geese slept 1.5 h less per day in summer compared with winter. In both seasons, the amount of NREM sleep was additionally affected by the lunar cycle, with 2 h NREM sleep less during full moon compared to new moon. During summer, the geese responded to 4 and 8 h of sleep deprivation with a compensatory increase in NREM sleep time. In winter, this homeostatic response was absent. Overall, sleep deprivation only resulted in minor changes in the spectral composition of the sleep EEG. In conclusion, barnacle geese display season-dependent homeostatic regulation of sleep. These results demonstrate that sleep homeostasis is not a rigid phenomenon and suggest that some species may tolerate sleep loss under certain conditions or during certain periods of the year.

Urban noise restricts, fragments, and lightens sleep in Australian magpies.

Urban areas are inherently noisy, and this noise can disrupt biological processes as diverse as communication, migration, and reproduction. We investigated how exposure to urban noise affects sleep, a process critical to optimal biological functioning, in Australian magpies (Cracticus tibicen). Eight magpies experimentally exposed to noise in captivity for 24-h spent more time awake, and less time in non-rapid eye movement (non-REM) and REM sleep at night than under quiet conditions. Sleep was also fragmented, with more frequent interruptions by wakefulness, shorter sleep episode durations, and less intense non-REM sleep. REM sleep was particularly sensitive to urban noise. Following exposure to noise, magpies recovered lost sleep by engaging in more, and more intense, non-REM sleep. In contrast, REM sleep showed no rebound. This might indicate a long-term cost to REM sleep loss mediated by noise, or contest hypotheses regarding the functional value of this state. Overall, urban noise has extensive, disruptive impacts on sleep composition, architecture, and intensity in magpies. Future work should consider whether noise-induced sleep restriction and fragmentation have long-term consequences.

White and Amber Light at Night Disrupt Sleep Physiology in Birds.

Artificial light at night can disrupt sleep in humans [1-4] and other animals [5-10]. A key mechanism for light to affect sleep is via non-visual photoreceptors that are most sensitive to short-wavelength (blue) light [11]. To minimize effects of artificial light on sleep, many electronic devices shift from white (blue-rich) to amber (blue-reduced) light in the evening. Switching outdoor lighting from white to amber might also benefit wildlife [12]. However, whether these two colors of light affect sleep similarly in different animals remains poorly understood. Here we show, by measuring brain activity, that both white and amber lighting disrupt sleep in birds but that the magnitude of these effects differs between species. When experimentally exposed to light at night at intensities typical of urban areas, domestic pigeons (Columba livia) and wild-caught Australian magpies (Cracticus tibicen tyrannica) slept less, favored non-rapid eye movement (NREM) sleep over REM sleep, slept less intensely, and had more fragmented sleep compared to when lights were switched off. In pigeons, these disruptive effects on sleep were similar for white and amber lighting. For magpies, however, amber light had less impact on sleep. Our results demonstrate that amber lighting can minimize sleep disruption in some birds but that this benefit may not be universal. VIDEO ABSTRACT.