Sleep and Wakefulness

Circadian Rhythm

An endogenous biological mechanism that occurs on a regular pattern about every 24 hours (e.g., the sleep-wake cycle and body temperature)

Endogenous Rhythms

Self-generated rhythms that range in length. Circadian rhythms (daily) differ from others like circannual rhythms (yearly)

Evidence of Existence

Experiments with animals (like hamsters) in constant dim light show they maintain a regular rhythm, though it may drift a few minutes later each day (free-running)

Suprachiasmatic Nucleus (SCN)

Part of the hypothalamus located above the optic chaism; it is the main driver of the circadian rhythms

Proof of SCN Function

Lesions to the SCN cause an animal’s activity to become completely random in constant dim light, indicating the loss of the endogenous rhythm

Molecular Mechanism

Oscillations of mRNA and protein concentrations (e.g., PER for “period” and TIM for “timeless”). High levels of PER and TIM proteins inhibit the gene transcription that produces them, creating a feedback loop

Entrainment

The process of synchronizing a biological rhythm to an environmental stimulus (Zeitgeber). Light resets the clock via the retinohypothalamic tract, where specialized melanopsin-containing retinal ganglion cells respond to average light levels (especially BLUE LIGHT).

Melatonin

A hormone that increases sleepiness; it is released by the pineal gland under the control of the SCN

Stage 1

Light sleep characterized by theta waves

Stage 2

Light sleep featuring sleep spindles (short bursts of waves) and K-complexes

Stages 3 & 4 (Slow-Wave Sleep/SWS)

Deep sleep characterized by high-amplitude, low-frequency delta waves

REM (Rapid Eye Movement)

Also called paradoxical sleep; the EEG looks like wakefulness, but the body experiences muscle atonia (PARALYSIS). It is associated with vivid dreams

Typical Progression

Sleepers move through stages 1→2→3→4, then cycle back from 4→3→2→REM

Cycles

Each cycle lasts approximately 90 minutes; humans typically cycle 4-5 times per night

Timing

SWS (Stages 3&4) predominates early in the night, while REM sleep length increases predominates later in at night

Basal Forebrain

Promotes SWS by releasing GABA; lesions here cause insomnia

Reticular Formation (Brainstem)

Projects axons to activate the forebrain into wakefulness and alertness

Pons (near Locus Coeruleus)

triggers REM sleep and inhibits motor neurons to cause muscle atonia

Hypothalamus (Orexin/Hypocretin System)

Neurons using orexin (hypocretin) coordinate the other centers to maintain organized sleep and wakefulness

Sleep Apnea

Disrupted breathing during sleep due to airway obstruction; treated with weight loss, avoiding alcohol, or CPAP macines

Narcolepsy

Sudden attacks of sleepiness and cataplexy (loss of muscle tone). It is caused by a loss of orexin/hypocretin neurons. Treatments include stimulants or antidepressants

Energy Conservation Sleep Theory

SWS reduces metabolic activity, heart rate, and body temperature

Niche Adaptation Theory

Natual selection enforces sleep at the most dangerous or least productive times of day

Body Restoration

Sleep is needed for growth, immune function, and metabolite clearance (e.g., clearing amyloid beta)

Restoration of Mind Theory

Sleep derivation impairs concentration and performance

Memory Consolidation Theory

Sleep aids memory by mimicking task activity (faster) and strengthening synaptic connections. Sleep spindles increase in number after learning