CHAPTER 9: RHYTHMS OF WAKEFULNESS AND SLEEP

A. Endogenous circannual rhythm: An internal calendar which prepares a species for

annual seasonal changes.

B. Endogenous circadian rhythm: Internal rhythms which last about a day (e.g.,

wakefulness and sleepiness).

C. Biological clock: An internal mechanism which controls behavior that is exhibited on a regular schedule.

1. Our biological clock has a free-running rhythm of about 24 1/2 to 24 3/4 hours per day.

2. A zeitgeber (e.g., light), is necessary for resetting the biological clock.

3. Researchers who have attempted to alter the biological clock believe it is difficult

for humans to adjust to a wake-sleep cycle different from 24 hours per day.

D. Jet lag: A disruption of our biological rhythms due to crossing time zones (e.g., traveling east, we tend to sleep and awaken earlier than usual).

E. Night shift workers often have difficulty adjusting to their wake/sleep cycle (e.g., waking up groggy, not sleeping well during the day, etc.). Working under very bright lights and sleeping in a very dark room may help shift the circadian rhythms.

F. Suprachiasmatic nucleus (SCN): Located above the optic chiasm in the hypothalamus. The SCN controls the rhythms for sleep and temperature.

1. The neurons of the SCN generate impulses that follow a circadian rhythm.

2. In flies and mice, the SCN regulates the circadian rhythms through the regulation of two genes, period and timeless. Early in the morning the concentration of both gene products are low and they increase during the day. In the evening protein concentrations are high and result in sleepiness. During the night the genes stop producing the proteins.

3. The SCN is reset by the retinohypothalamic path that extends directly from the retina to the SCN

G. Melatonin: Released by the pineal gland, mainly at night, is a hormone that increases sleepiness. Melatonin release usually starts 2 or 3 hours before bedtime. 1. Melatonin stimulates receptors in the SCN to reset the biological clock.

A..Stages of Sleep

1. The electroencephalograph (EEG) records gross electrical potentials in an area of the brain by attaching an electrode to the scalp.

2. Alpha waves have a frequency of about 8-12 brain waves per second; these waves are typical of a relaxed state of consciousness.

3. Stage 1 sleep is a stage of light sleep noted by the presence of irregular, jagged, low-voltage waves.

4. Stage 2 sleep is characterized by sleep spindles (a burst of 12-14 Hz waves which last approximately one-half second) and K-complexes (sharp, high-amplitude waves followed by a smaller, positive wave).

5. Stages 3 and 4 sleep are known as slow-wave sleep (SWS) which are comprised of slow, large amplitude waves.

6. When people fall asleep, they enter stage 1 followed by stages 2, 3 and 4, in that order. Approximately 60-90 minutes after falling asleep, they cycle back from stage 4 through stages 3, 2 and then enter rapid eye movement (REM) sleep.

7. Rapid eye movement (REM) sleep: Also known as paradoxical sleep, is a period of sleep characterized by repeated eye movements, fast low-voltage brain waves, plus breathing and heart rates similar to stage 1 sleep. REM sleep is associated with dreaming but dreams can happen in non-REM sleep (e.g. stages 1-4).

8.Polysomnograph: A combination of EEG and eye-movement records.

9. After entering REM sleep, the sleep cycle sequence repeats with each complete cycle lasting 90 minutes.

10. REM states are associated with "loose" association or thinking.

B. Brain Structures of Arousal

1. Reticular formation: A structure that extends from the medulla into the forebrain. Lesions through the reticular formation decrease arousal.

2. Pontomesencephalon: A part of the reticular formation that contributes to cortical arousal. Stimulation of the pontomesencephalon awakens a sleeping individual or increases alertness in someone already awake.

3. Locus Coeruleus: A structure in the pons that emits impulses, releasing norepinephrine, in response to meaningful events. The locus coeruleus is also important for storing information in genes of activated cells.

4. Basal forebrain: An area just anterior and dorsal to the hypothalamus whose axons release acetylcholine. Damage to the basal forebrain leads to decreased arousal, impaired learning and attention and more time spent in non-REM sleep.

5. Certain areas of the hypothalamus stimulate arousal by releasing histamine. Antihistamine drugs produce drowsiness if they cross the blood-brain barrier.

C. Getting to Sleep

1. Adenosine: An important inhibitor of the basal forebrain arousal system. Caffeine increases arousal by inhibiting adenosine.

2. Prostaglandins: Chemical that promote sleep by stimulating a cluster of neurons that inhibit the hypothalamic cells that increase arousal.

3. Certain basal forebrain cells release GABA and promote sleepiness. The sleep- related basal forebrain cells get their input from the anterior and preoptic areas of the hypothalamus (areas important for temperature regulation).

D. Brain Function in REM Sleep

1. PGO (Pons-geniculate-occipital) waves: A distinctive pattern of high-amplitude electrical potentials associated with REM sleep. The waves are detected first in the pons, shortly afterward in the lateral geniculate nucleus of the thalamus, and then in the occipital cortex.

2. The pons also relay messages to inhibit motor neurons in the spinal cord during REM sleep.

3. REM sleep depends on both serotonin and acetylcholine activity for its onset and continuation. Stimulation of acetylcholine synapses quickly moves a sleeper into REM and serotonin interrupts or shortens REM sleep.

E. Abnormalities of sleep

1. Insomnia: Problems falling asleep or to maintaining sleep. There are three categories of insomnia:

Onset insomnia: Trouble falling asleep.

Maintenance insomnia: Waking up frequently during the night after falling asleep.

Termination insomnia: Waking up too early and can not go back to sleep. Insomnia may be due to biological rhythm abnormalities (e.g., trying to sleep while body temperature rises), or the use of sleeping pills.

2. Sleep Apnea: Inability to breath during sleep; obesity is a common cause of this disorder, particularly in men. It is a possible cause of sudden infant death syndrome.

3. Narcolepsy: Frequent unexpected periods of sleepiness during the day. Symptoms include gradual or sudden attacks of sleepiness, cataplexy (attack of muscle weakness while awake), sleep paralysis (inability to move while asleep), and hypnagogic hallucination (dream like experiences occurring at the onset Of sleep). Each of these symptoms is interpreted as REM sleep intruding into wakefulness; this disorder is often treated with stimulant medication.

4. Periodic limb movement disorder: Repeated involuntary movements of the legs and arms; occurs mostly during NREM sleep. This disorder is often treated with tranquilizers.

5. REM behavior disorder: Disorder where people move around vigorously during their REM periods apparently acting out their dreams. Likely due to the inability of the pons to inhibit spinal motor neurons.

6. Night terrors: An abrupt, anxious awakening from NREM sleep; this disorder is more common in children than adults.

7. Sleep talking: May occur during either REM or NREM sleep.

8. Sleepwalking: Usually occurs during stages 3 or 4 early in the night and is more common in children than adults.

A. Repair and Restoration Theory of Sleep: The body, especially the brain, requires sleep to repair itself after the exertions of the day.

B. Evolutionary Theory of Sleep: We sleep to save energy when we otherwise should be energy inefficient, such as during the night.

C. Human infants spend more time in REM sleep than do adults suggesting that REM may be important for modifying neuronal connections in response to early experience.

D. Because adults who get the most sleep have the most REM sleep and adults who get the least sleep get the least amount of REM, NREM sleep seems to be more of a biological need while REM sleep is optional.

E. REM sleep deprivation leads to increased attempts at REM sleep.

F. REM sleep has been implicated in memory storage and as a way of getting oxygen to the corneas.

G. Activation-synthesis hypothesis: During sleep, many brain regions become activated, so the brain creates a story to make sense of all this activity.

H. Clinico-Anatomical Hypothesis: Either internal or external stimulation activates parts of the parietal, occipital, and temporal cortex. No visual information overrides the stimulation and no criticism of the prefrontal cortex censors it, so it develops into hallucinatory perceptions.