NEU200: Unit 3 Key Terms

Circadian Cycle

An endogenous biological rhythm that follows an approximately 24-hour cycle. Circadian rhythms persist even when an organism is isolated from normal day–night cues, showing that they are generated internally rather than created entirely by the environment. They influence sleep–wake timing, body temperature, hunger, and hormone secretion. Environmental cues such as light, noise, and temperature can influence or reset these rhythms.

Pineal Gland (“Third Eye” in Reptiles and Amphibians)

An endocrine gland that produces melatonin, a hormone involved in circadian timing. In mammals, light information reaches the brain through the eyes and influences pineal activity. In some non-mammalian vertebrates, including certain reptiles and amphibians, the pineal gland can respond more directly to light, giving rise to the historical term “third eye.”

Melatonin

A hormone produced by the pineal gland that helps signal biological night and regulate circadian timing. Melatonin levels generally rise in darkness and are suppressed by light. It helps coordinate the timing of sleep with the light–dark cycle; it should not be understood as an on/off switch that directly causes sleep.

Suprachiasmatic Nucleus (SCN)

A nucleus in the hypothalamus located above the optic chiasm, where the optic nerves cross. It receives light-related information from the eyes and acts as a major endogenous circadian clock. The SCN helps synchronize internal rhythms with the external day–night cycle. If the SCN is damaged, animals can still sleep, but their sleep–wake patterns become less organized. Transplantation studies described in the lecture show that a transplanted SCN can impose its donor's circadian timing on the recipient.

Electroencephalogram (EEG)

A method of recording the brain's electrical activity using electrodes placed on the scalp. An EEG reveals patterns that differ across wakefulness and sleep. These patterns are distinguished by their frequency, amplitude, and degree of synchronization. The lecture uses EEG waves to identify alert wakefulness, quiet resting, and the different sleep stages.

Awake State

A state of wakefulness associated in the lecture with relatively fast beta waves, approximately 24–30 Hz. Beta activity is associated with alertness and active information processing. It contrasts with the slower alpha waves of quiet resting and the progressively slower theta and delta activity seen during sleep.

Quiet Resting

A relaxed but awake state associated with alpha waves, approximately 8–13 Hz. Compared with the beta activity associated with alert wakefulness, alpha activity is slower and is described in the lecture as more synchronized. Quiet resting is still wakefulness, not a sleep stage.

Stage 1 Sleep (Theta Waves)

The lightest stage of non-REM sleep in the lecture's traditional four-stage classification. It is associated with theta waves, approximately 4–7 Hz, as brain activity slows during the transition from wakefulness into sleep. It is relatively light sleep compared with the deeper stages.

Stage 2 Sleep (Theta Waves + Sleep Spindles)

A non-REM sleep stage characterized by theta activity and sleep spindles: brief bursts of intense, high-frequency EEG activity. Sleep spindles are an important feature distinguishing Stage 2 from the simpler theta-wave pattern described for Stage 1.

Stage 3 Sleep (Delta Waves)

A deep non-REM sleep stage characterized by slow delta waves, approximately 0.5–3 Hz. These waves have high amplitude and reflect relatively synchronized activity across neuronal populations. Stage 3 is part of deep, slow-wave sleep and is generally harder to awaken from than lighter sleep stages.

Stage 4 Sleep (Delta Waves)

The deepest stage in the lecture's traditional four-stage classification. EEG activity is dominated by slow delta waves, with faster wave patterns reduced relative to lighter stages. Stages 3 and 4 both represent deep, slow-wave sleep. The lecture uses the traditional four-stage system, so retain that terminology for this course.

REM Sleep / Paradoxical Sleep

REM stands for rapid eye movement. REM is called paradoxical sleep because the brain displays relatively fast, wake-like electrical activity while most skeletal muscles are inhibited. The lecture associates REM with beta-like EEG activity, vivid dream reports, and muscle paralysis caused by descending brainstem pathways. Dreaming is not exclusive to REM, but people often report their most detailed dreams when awakened from REM.

REM Rebound

The increase in REM sleep that can occur after REM has been repeatedly interrupted or prevented. In the lecture's example, a person is awakened whenever REM begins; on a subsequent night, the person compensates by spending more time in REM. The notes emphasize that this selective rebound suggests REM serves an important biological function, although it does not establish exactly what that function is.

Memory Consolidation as a Possible Function of REM

The hypothesis that REM sleep contributes to stabilizing, organizing, or integrating memories. The lecture presents this as a possible function, not a proven or exclusive purpose of REM. The notes point out that people with impairments affecting dreaming can still learn, so dreaming and the ability to form memories should not be treated as identical. Other possibilities raised in the lecture include temperature regulation and the need to maintain brain activity.

Ascending Reticular Activating System (ARAS; Medulla)

A brainstem system associated in the lecture with the medulla that helps maintain wakefulness and alertness. It receives input from multiple sources, including information related to internal timing and activity elsewhere in the brain, and sends activating signals to the rest of the brain. The lecture's lesion evidence suggests that the ARAS is necessary for sustained wakefulness: damage can prevent the brain from staying awake and may produce a sleep-like state or coma.

Pontine Reticular System (PRS)

A system in the pons involved in brainstem activation, reflexes, and REM sleep. The lecture distinguishes an ascending pathway associated with REM-related activation and dream experiences from a descending pathway that inhibits spinal motor activity during REM. Together, these pathways help explain how the brain can remain active during REM while the body is largely prevented from acting out dreams.

Ascending Pontine Reticular System

The ascending component of the pontine reticular system, described in the lecture as contributing to REM-related brain activity and dream generation. Activity from the pons can travel toward the thalamus and influence the cortex. The lecture proposes that internally generated neural signals are processed by these higher brain regions and contribute to dream experiences. The pons does not itself create complete dream images; rather, its activity supplies signals that other brain regions process.

Descending Reticular System (DRS)

The descending component of the reticular system that inhibits spinal motor activity during REM sleep. This inhibition produces muscle atonia, keeping most skeletal muscles from carrying out dream-related actions while the brain remains active. In the lecture's animal-lesion example, damage to the descending pathway allows cats to display movements resembling dream enactment during REM, supporting the pathway's role in normal REM-related muscle inhibition.