the brain in a highly speciﬁ c manner, forming a ﬁ ber system
known as the reticular formation, also sometimes called the
reticular activating system (RAS).
This system is, in fact,
composed of several separate divisions, distinguished by their
anatomical distribution and neurotransmitters. The divisions
originate in different nuclei within the brainstem, and some of
them send ﬁ
bers to those areas of the thalamus that inﬂ uence
the EEG. Components of the RAS that release norepineph-
rine, serotonin, or acetylcholine—functioning in this instance
more as neuromodulators—are most involved in controlling
the various states of consciousness.
One hypothesis about how sleep-wake cycles are gener-
ated proposes that alternating reciprocal activity of different
types of neurons in the RAS causes shifts from one state to
the other. In this model (
), the waking state and
REM sleep are at opposite ends of a spectrum: During wak-
ing, the aminergic neurons (those that release norepinephrine
or serotonin) dominate, and during REM sleep the cholin-
ergic neurons are dominant. NREM sleep, according to this
model, is intermediate between the two extremes.
The aminergic neurons, which are active during the wak-
ing state, facilitate a state of arousal, enhancing both attention
to perceptions of the outer world and the motor activity that
characterizes awake behavior. These neurons also inhibit cer-
tain of the cholinergic brainstem neurons. As the aminergic
neurons stop ﬁ ring, the cholinergic neurons, released from
inhibition, increase their activity.
There are two additional areas in the forebrain (
) that are involved in the control of sleep-wake cycles. The
preoptic area of the hypothalamus promotes slow-wave sleep
by inhibitory GABAergic inputs to the thalamocortical neu-
rons and to the midbrain reticular formation. It also inhib-
its activity within a center in the posterior hypothalamus that
stimulates wakefulness. These latter neurons use histamine
as a neurotransmitter and they also project to the RAS. The
drowsiness that occurs in people using antihistamines may be
a result of blocking the histaminergic transmission originat-
ing in the posterior hypothalamus.
Finally, the basic rhythm of the sleep-wake cycle is inﬂ u-
enced by the biological clock function of the suprachias-
matic nucleus. This nucleus of the hypothalamus regulates
the timing of sleep and awake periods relative to periods of
light and darkness, that is, the circadian rhythm (Chapter
1) of the states of consciousness. The nucleus stimulates the
pineal gland’s production of melatonin (Chapters 1 and 11).
Although melatonin has been used as a “natural” substance
EEG (See Figures 8–3 and 8–4)
Awake, alert with eyes open.
Beta rhythm (faster than 13 Hz).
Awake, relaxed with eyes closed.
Mainly alpha rhythm (8–13 Hz) over the
parietal and occipital lobes. Changes to beta
rhythm in response to internal or external
Fatigued, tired, or bored; eyelids may narrow and close;
head may start to droop; momentary lapses of attention
and alertness. Sleepy but not asleep.
Decrease in alpha-wave amplitude and
NREM (slow-wave) sleep
Light sleep; easily aroused by moderate stimuli or
even by neck muscle jerks triggered by muscle stretch
receptors as head nods; continuous lack of awareness.
Alpha waves reduced in frequency, amplitude,
and percentage of time present; gaps in alpha
rhythm ﬁ lled with theta (4–8 Hz) and delta
(slower than 4 Hz) activity.
Further lack of sensitivity to activation and arousal.
Alpha waves replaced by random waves of
Stages 3 and 4
Deep sleep; in stage 4, activation and arousal occur only
with vigorous stimulation.
Much theta and delta activity, predominant
delta in stage 4.
REM (paradoxical) sleep
Deepest sleep; greatest relaxation and difﬁ culty of
arousal; begins 50–90 min after sleep onset, episodes
repeated every 60–90 min, each episode lasting about
10 min; dreaming occurs, rapid eye movements behind
closed eyelids; marked increase in brain O
EEG resembles that of alert awake state.