Neuroscience of Sleep-Wake Regulation

A hypothetical substance that, when present, promotes sleep and, when inhibited, reduces sleep. This substance's levels should correlate with the urge to sleep and be affected by sleep deprivation. It's likely to act on neural pathways involved in sleep regulation.

The process by which the body builds up a 'sleep debt' during wakefulness and then pays it off by sleeping. It's like an hourglass, with 'sand' accumulating during wakefulness and slowly emptying during sleep.

A molecule that increases in the brain during wakefulness. It's a strong candidate for a "sleep regulatory substance" and might be involved in the sleep drive.

Electroencephalography, a neuroimaging technique used to measure and record the brain's electrical activity, mainly from the outer layer of the brain, the cerebral cortex.

The different states of wakefulness, non-REM sleep, and REM sleep, each with its own distinct electrical brainwave pattern. This is what scientists use to differentiate between sleeping stages.

Synchronized electrical activity in the brain, creating larger, more noticeable EEG signal amplitudes. This usually indicates a deeper stage of sleep.

A graphical representation of the different sleep stages over time. It gives scientists a picture of a person's overall sleep 'architecture'.

The group of interconnected brain areas that control the transition between different sleep and wake states. It dictates when you fall asleep and when you wake up.

The medulla and pons, two brain stem structures crucial for regulating sleep and wakefulness. They are involved in managing basic functions, like breathing and heart rate, and also play a role in sleep.

Neurons in the lateral hypothalamus (LH) release orexin which excites neurons in the cortex, thalamus, and all wake-promoting brain regions.

Activation of orexin neurons helps animals wake up from sleep and suppresses REM sleep.

Loss of orexin neurons does not impact the total amount of sleep or wakefulness, but it causes more frequent transitions between sleep states.

Restoring the activity of the tuberoinfundibular nucleus (TMN) and locus coeruleus (LC) significantly improves the ability to stay awake after orexin loss.

Inhibiting the locus coeruleus (LC) blocks the awakening effect of stimulating orexin neurons during sleep.

Lesions to the lateral hypothalamus cause more severe sleepiness symptoms than just losing orexin neurons.

GABAergic neurons located in the ventrolateral preoptic nucleus (VLPO) and median preoptic nucleus (MNPO) promote non-REM sleep by inhibiting wake-promoting neurons.

The basal forebrain contains GABAergic sleep-active neurons that may promote sleep.

GABAergic neurons in the parafacial zone may promote sleep by inhibiting the parabrachial nucleus.

Different neural circuitry controls REM sleep, including neurons in the sublaterodorsal (SLD) nucleus, PPT/LDT, and the lateral hypothalamus.

A group of interconnected brain regions that regulate the transitions between sleeping and waking states.

Neurochemicals like dopamine, serotonin, and norepinephrine that influence wakefulness, often showing higher activity during wakefulness and lower activity during sleep.

A group of neurons located in the brainstem that promotes wakefulness by activating other brain regions.

Neurons in the basal forebrain that are particularly active during wakefulness and REM sleep, promoting fast brain waves and a more active state.

Wake-promoting chemicals that tend to activate thalamic relay neurons, contributing to the awake brain state.

A state of wakefulness characterized by coordinated activity, attentive behavior, and responsiveness to the environment.

The difficulty in understanding the precise function of a brain area due to its potential involvement in many different aspects of wakefulness.

The challenge of determining whether a brain region's function is primary or a consequence of other activated pathways.

The significant variety of cell types and their connections within a single brain region, making it difficult to understand their individual roles.

The inherent difficulty of understanding the contributions of multiple brain regions simultaneously, as their combined activity likely creates emergent behavioral states.

A rhythmic biological process within a 24-hour cycle, influencing our behavior and physiology. Think of it as a natural clock within us, which, for example, regulates when we feel tired and sleepy.

A cluster of brain cells in the hypothalamus, known as the master clock. This tiny area serves as the central pacemaker for our circadian rhythms, receiving information about light and darkness.

The SCN neurons generate cyclical electrical activity with a 24-hour period. Think of it like a rhythmic electrical signal that keeps time.

Proteins within the SCN cells interact in a loop that takes about 24 hours to complete, influencing the SCN's rhythm. This cycle is crucial for maintaining the SCN's time-keeping function.

Light triggers the release of chemicals from the retina, which reach the SCN via specific neural pathways, influencing the SCN's activity and shifting our internal clock.

A physiological process where our body builds up a 'sleep debt' throughout the day, which needs to be repaid during sleep. It's like an imaginary hourglass where the 'sand' represents sleepiness.

The urge to sleep, which increases as we stay awake longer. This reflects our body's way of urging us to restore lost sleep.

The process of synchronizing our internal clock with the external environment. This allows us to align our sleep-wake cycle with the day-night cycle.

Disruptions in our sleep-wake cycle, resulting in poor sleep quality or disrupted sleep patterns. This can be caused by factors like shift work, jet lag, or unhealthy lifestyle choices.

The process of falling asleep and transitioning through different sleep stages. This involves distinct brainwave patterns.