Individualized temporal patterns drive human sleep spindle timing.

Sleep spindles are cortical electrical oscillations considered critical for memory consolidation and sleep stability. The timing and pattern of sleep spindles are likely to be important in driving synaptic plasticity during sleep as well as preventing disruption of sleep by sensory and internal stimuli. However, the relative importance of factors such as sleep depth, cortical up/down-state, and temporal clustering in governing sleep spindle dynamics remains poorly understood.

Evo-devo applied to sleep research: an approach whose time has come.

Sleep occurs in all animals but its amount, form, and timing vary considerably between species and between individuals. Currently, little is known about the basis for these differences, in part, because we lack a complete understanding of the brain circuitry controlling sleep-wake states and markers for the cell types which can identify similar circuits across phylogeny. Here, I explain the utility of an "Evo-devo" approach for comparative studies of sleep regulation and function as well as for sleep medicine.

Sleep-Deep-Learner is taught sleep-wake scoring by the end-user to complete each record in their style.

Sleep-wake scoring is a time-consuming, tedious but essential component of clinical and preclinical sleep research. Sleep scoring is even more laborious and challenging in rodents due to the smaller EEG amplitude differences between states and the rapid state transitions which necessitate scoring in shorter epochs. Although many automated rodent sleep scoring methods exist, they do not perform as well when scoring new datasets, especially those which involve changes in the EEG/EMG profile.

Individualized temporal patterns dominate cortical upstate and sleep depth in driving human sleep spindle timing.

Sleep spindles are critical for memory consolidation and strongly linked to neurological disease and aging. Despite their significance, the relative influences of factors like sleep depth, cortical up/down states, and spindle temporal patterns on individual spindle production remain poorly understood. Moreover, spindle temporal patterns are typically ignored in favor of an average spindle rate.

Sleep-Deep-Net learns sleep wake scoring from the end-user and completes each record in their style.

Sleep-wake scoring is a time-consuming, tedious but essential component of clinical and pre-clinical sleep research. Sleep scoring is even more laborious and challenging in rodents due to the smaller EEG amplitude differences between states and the rapid state transitions which necessitate scoring in shorter epochs. Although many automated rodent sleep scoring methods exist, they do not perform as well when scoring new data sets, especially those which involve changes in the EEG/EMG profile.

Alterations of sleep oscillations in Alzheimer's disease: A potential role for GABAergic neurons in the cortex, hippocampus, and thalamus.

Sleep abnormalities are widely reported in patients with Alzheimer's disease (AD) and are linked to cognitive impairments. Sleep abnormalities could be potential biomarkers to detect AD since they are often observed at the preclinical stage. Moreover, sleep could be a target for early intervention to prevent or slow AD progression.

Characterization of basal forebrain glutamate neurons suggests a role in control of arousal and avoidance behavior.

The basal forebrain (BF) is involved in arousal, attention, and reward processing but the role of individual BF neuronal subtypes is still being uncovered. Glutamatergic neurons are the least well-understood of the three main BF neurotransmitter phenotypes. Here we analyzed the distribution, size, calcium-binding protein content and projections of the major group of BF glutamatergic neurons expressing the vesicular glutamate transporter subtype 2 (vGluT2) and tested the functional effect of activating them.

Basal Forebrain Parvalbumin Neurons Mediate Arousals from Sleep Induced by Hypercarbia or Auditory Stimuli.

The ability to rapidly arouse from sleep is important for survival. However, increased arousals in patients with sleep apnea and other disorders prevent restful sleep and contribute to cognitive, metabolic, and physiologic dysfunction [1, 2]. Little is currently known about which neural systems mediate these brief arousals, hindering the development of treatments that restore normal sleep.

Thalamic Reticular Nucleus Parvalbumin Neurons Regulate Sleep Spindles and Electrophysiological Aspects of Schizophrenia in Mice.

The thalamic reticular nucleus (TRN) is implicated in schizophrenia pathology. However, it remains unclear whether alterations of TRN activity can account for abnormal electroencephalographic activity observed in patients, namely reduced spindles (10-15 Hz) during sleep and increased delta (0.5-4 Hz) and gamma-band activity (30-80 Hz) during wakefulness.

Validation of an automated sleep spindle detection method for mouse electroencephalography.

Study Objectives: Sleep spindles are abnormal in several neuropsychiatric conditions and have been implicated in associated cognitive symptoms. Accordingly, there is growing interest in elucidating the pathophysiology behind spindle abnormalities using rodent models of such disorders. However, whether sleep spindles can reliably be detected in mouse electroencephalography (EEG) is controversial necessitating careful validation of spindle detection and analysis techniques.

Activation of basal forebrain purinergic P2 receptors promotes wakefulness in mice.

The functions of purinergic P2 receptors (P2Rs) for extracellular adenosine triphosphate (ATP) are poorly understood. Here, for the first time, we show that activation of P2Rs in an important arousal region, the basal forebrain (BF), promotes wakefulness, whereas inhibition of P2Rs promotes sleep. Infusion of a non-hydrolysable P2R agonist, ATP-γ-S, into mouse BF increased wakefulness following sleep deprivation.

The menagerie of the basal forebrain: how many (neural) species are there, what do they look like, how do they behave and who talks to whom?

The diverse cell-types of the basal forebrain control sleep-wake states, cortical activity and reward processing. Large, slow-firing, cholinergic neurons suppress cortical delta activity and promote cortical plasticity in response to reinforcers. Large, fast-firing, cortically-projecting GABAergic neurons promote wakefulness and fast cortical activity.

Intrinsic membrane properties and cholinergic modulation of mouse basal forebrain glutamatergic neurons in vitro.

The basal forebrain (BF) controls sleep-wake cycles, attention and reward processing. Compared to cholinergic and GABAergic neurons, BF glutamatergic neurons are less well understood, due to difficulties in identification. Here, we use vesicular glutamate transporter 2 (vGluT2)-tdTomato mice, expressing a red fluorescent protein (tdTomato) in the major group of BF glutamatergic neurons (vGluT2+) to characterize their intrinsic electrical properties and cholinergic modulation.