Module 4: Physiology of sleep and arousal

➢ Arousal
➢ Physiological measures of alertness and arousal-EEG
➢ Physiological conceptions of wakefulness and sleep
➢ Conceptions of sleep
➢ Circadian rhythms and biological clock

Arousal is defined as the state of awakening of sense organs up to the point where sensation
and perception can take place. There is an activation of various mechanisms, such as
reticulate activating system which increases wakefulness, functioning of autonomic nervous
system as well as endocrine system. The functioning of these mechanisms also increases
ability to respond more quickly and higher alertness. The physiological aspect of arousal
looks at how wakefulness is achieved through arousal. Research points towards the
functioning of ascending reticulate system which consists of a number of neurotransmitters
(acetylcholine, norepinephrine, dopamine, histamine, and serotonin). All these
neurotransmitters play a crucial role in the arousal activity. There are numerous correlations
of arousal which are related to emotional, sexual, mood, sleep, and temperament.

Numerous researches have been done to understand the physiological correlates of arousal.
Arousal occurs in different mechanisms and across different bodily functions. Some of these
mechanisms and bodily functions include emotional arousal, sleep arousal, sexual arousal,
mood and affect arousal, and cardiovascular functioning.

The physiological correlates of arousal are measured on numerous neurophysiological

assessment mechanisms, such as EEG, EKG, PET scan and fMRI. Results of these reviews
indicated that the physiological correlates of arousal are related to changes in the functioning
of body mechanisms such as cardiovascular systems, breathing and heart rate, nervous system
and reaction to various types of stimuli. It also involves changes in the functioning of certain
brain areas and influences temperament as well.

PHYSIOLOGICAL MEASURES OF ALERTNESS AND AROUSAL

Transient increase in alertness is most often examined in terms of a phenomenon called the
orientation reaction. The specific responses that collectively represent the orientation
reaction are called orienting responses (ORs).
The phenomenon was first described by Russian physiologist E.N Sokolov in 1963 and the
term was coined by Ivan Pavlov.
Each OR can be viewed as a general readiness of the animal to act and to react, when the
stimulus presented is novel in some way. When the stimulus event is repeated, its novelty is
naturally reduced. Then the magnitude of the OR diminishes until it does not occur at all, in a
process called OR habituation.
The ORs in an orientation reaction or orienting reflex are; the pupil widens, respiration
rate and heart rate decelerate, blood vessels in the limbs constrict, muscle activity increases,
head movements and eye movements toward the source of stimulus, a pricking up of the ears
(in animals), eye widening and a reduction in salivation.
Researchers have found a number of physiological responses associated with orientation
reaction, including:
(i) Skin resistance response (SSR) – an increase in sweat gland activity in the skin causing a
fall in skin resistance
(ii) Skin conductance response (SCR) – lower level of skin resistance during orientation
reaction is referred to as a rise in skin conductance.
(iii) Electroencephalogram (EEG) – The wave pattern prior to the stimulus event is called
alpha (moderate amplitude waves with a frequency between 8 and 13 Hz). The wave pattern
subsequent to the event is called beta (low amplitude waves with frequency between 14 and
26 Hz). The transition between alpha and beta EEG patterns is referred to as alpha blocking
or cortical desynchronisation (since beta waves are less synchronized than alpha waves).

THE EEG AS A MEASURE OF AROUSAL

The EEG is a record of the changing voltage in brain tissue as monitored from the scalp, and
is usually defined in terms of the amplitude of its waves (1µV to 150µV) and the frequency
of the waves (0.5 Hz to 30 Hz).
On the basis of these dimensions, the EEG is categorised into three broad classes:
(i) Alpha waves - moderate amplitude waves with a frequency between 8 and 13 Hz
(ii) Beta waves - low amplitude waves with frequency between 14 and 26 Hz
(iii) Delta waves – high amplitude waves with frequency between 0.5 and 3.0 Hz

MEASURING SLEEP IN LABORATORY

Laboratory sleep studies allow researchers to measure sleep accurately and to record
physiological changes associated with sleep.

The principal monitoring systems:

(1) EEG (Electroencephalogram) for recording brain waves
(2) EOG (Electrooculogram) for measuring eye movements and
(3) EMG (Electromyogram) for measuring muscle tension on the chin.

STAGES OF SLEEP AS IN EEG

• The EEG recording shows distinct patterns of brain-wave activity as the neocortex
generates distinct rhythmic patterns from states categorized as awake, drowsy,
sleeping, and dreaming.
• A typical night’s sleep, as indicated by physiological measures, consists of stages that
take place in a number of cycles over the course of the night. During REM sleep, the
EEG has a waking pattern, and the sleeper displays rapid eye movements. Stages of
sleep in which the EEG has a slower rhythm are called non-REM (NREM) sleep.
• Sleep occurs in five stages: wake, N1, N2, N3, and REM. Stages N1 to N3 are
considered non-rapid eye movement (NREM) sleep, with each stage a progressively
deeper sleep. Approximately 75% of sleep is spent in the NREM stages, with the
majority spent in the N2 stage.[14] A typical night's sleep consists of 4 to 5 sleep
cycles, with the progression of sleep stages in the following order: N1, N2, N3, N2,
REM.
• A complete sleep cycle takes roughly 90 to 110 minutes. The first REM period is
short, and, as the night progresses, longer periods of REM and decreased time in deep
sleep (NREM) occur.
• Generally, four levels of sleep in NREM can be discriminated on the EEG record.
• Wake/Alert:

EEG recording: beta waves – highest frequency, lowest amplitude (alpha waves are
seen during quiet/relaxed wakefulness)

The initial position is the wake stage or stage W, which further depends on whether
the eyes are open or closed. During eye-open wakefulness, beta waves predominate.
As individuals become drowsy and close their eyes, alpha waves become the
predominant pattern.
• N1 (Stage 1) – Light Sleep (5%)

EEG recording: theta waves - low voltage

This is the lightest stage of sleep and begins when more than 50% of the alpha waves
are replaced with low-amplitude mixed-frequency (LAMF) activity. Muscle tone is
present in the skeletal muscle, and breathing tends to occur at a regular rate. This
stage lasts around 1 to 5 minutes, consisting of 5% of total sleep time.

• N2 (Stage 2) - Deeper Sleep (45%)

EEG recording: sleep spindles and K complexes

This stage represents deeper sleep as your heart rate and body temperate drop. It is
characterized by the presence of sleep spindles, K-complexes, or both.

Sleep spindles are brief, powerful bursts of neuronal firing in certain brain areas (the
superior temporal gyri, anterior cingulate, insular cortices, and thalamus, inducing
calcium influx into cortical pyramidal cells). This mechanism is believed to be
integral to synaptic plasticity. Numerous studies suggest that sleep spindles play an
important role in memory consolidation, specifically procedural and declarative
memory.

K-complexes are long delta waves that last for approximately one second and are
known to be the longest and most distinct of all brain waves. K-complexes have been
shown to function in maintaining sleep and memory consolidation.

Stage 2 sleep lasts around 25 minutes in the first cycle and lengthens with each
successive cycle, eventually consisting of about 45% of total sleep. This stage of sleep
is when bruxism (teeth grinding) occurs.

• N3 (Stage 3) - Deepest Non-REM Sleep (25%)

EEG recording: delta waves - lowest frequency, highest amplitude

N3 is also known as slow-wave sleep (SWS). This is considered the deepest stage of
sleep and is characterized by signals with much lower frequencies and higher
amplitudes, known as delta waves. This stage is the most difficult to awaken from,
 and, for some people, even loud noises (> 100 decibels) will not awaken them. As
people age, they tend to spend less time in this slow, delta wave sleep and more time
in stage N2 sleep.
Although this stage has the greatest arousal threshold, if someone is awoken during
this stage, they will have a transient phase of mental fogginess, known as sleep
inertia. Cognitive testing shows that individuals awakened during this stage tend to
have moderately impaired mental performance for 30 minutes to an hour. This is the
stage when the body repairs and regrows tissues, builds bone and muscle and
strengthens the immune system. This is also the stage when sleepwalking, night
terrors, and bedwetting occurs.

• Stage 4: N2

• REM (25%)

EEG recording: beta waves - similar to brain waves during wakefulness

REM is associated with dreaming and is not considered a restful sleep stage. While
the EEG is similar to an awake individual, the skeletal muscles are atonic and without
movement, except for the eyes and diaphragmatic breathing muscles, which remain
active. However, the breathing rate becomes more erratic and irregular.

This stage usually starts 90 minutes after you fall asleep, with each of your REM
cycles getting longer throughout the night. The first period typically lasts 10 minutes,
with the final one lasting up to an hour. REM is when dreaming, nightmares, and
penile/clitoral tumescence occur.

Important characteristics of REM:

• Associated with dreaming and irregular muscle movements as well as rapid
movements of the eyes
• A person is more difficult to arouse by sensory stimuli than during SWS
• People tend to awaken spontaneously in the morning during an episode of REM sleep
• Loss of motor tone, increased brain O2 use, increased and variable pulse and blood
pressure
• Increased levels of ACh.
• The brain is highly active throughout REM sleep, increasing brain metabolism by up
to 20%
Dissociations of EEG and behavioural arousal
• Dissociation occurs under the administration of certain anticholinergic drugs
(i) Drug atropine produces slow wave EEG (characteristic of behavioural sleep) when
the subject is behaviourally alert
(ii) Drug physostigmine produces low amplitude, fast activity in the EEG when the
subject is asleep.
• On a periodic basis during sleep- At regular intervals of sleep, the EEG changes from
delta frequencies to higher frequencies without any increase in the level of
behavioural arousal. (These periods are referred to as REM sleep)
PHYSIOLOGICAL CONCEPTIONS OF WAKEFULNESS AND SLEEP

The physiological basis for changes in arousal level was first thought to be a function of the
level of sensory input.
➢ The transection studies of Bremer (1935) suggested a sensory interpretation.

Experiment I: Encephale isole

Surgical procedure done (in observations conclusion

cat)
• Surgically separated the • Observations of the • Restricting the sensory
brain from spinal cord by pupils (dilation- input to merely the
severing the lower medulla wakefulness; and information carried by
• Most of the motor tracts are constriction – sleep) cranial nerves was
severed • EEG records showed the sufficient to sustain
alternating pattern of fast normal cycles of arousal
and slow waves
• The elimination of sensory
input from the body, as
mediated by the spinal
cord did not appear to
interfere with the casual
arousal patterns in the cat.

Experiment II: Cerveau isole

Surgical procedure done observations conclusion

Transection was made at the Changes in pupil size and Elimination of sensory input
level of the superior colliculus EEG activity observed; from most of the cranial
in the midbrain, thereby (i) EEG – a continuous slow nerves that have sensory
severing the brain from all wave and spindling pattern function was enough to cause
sensory input from spinal (ii) Pupil remained constricted the animal to lose its arousal
nerves and cranial nerves as in sleep state. capability.
except vision and smell.

➢ Studies of Moruzzi and Magoun (1949, showed that stimulation of the reticular
formation (in encephale isole) could produce EEG desynchronization common to
wakefulness, indicated that the input from the reticular formation to the entire
neocortex may underlie the maintenance of arousal.

➢ Supporting experiments:
Lindsley, Bowden, Magoun (1949) severed all the sensory nerves without damage to
the reticular formation and found normal wakefulness-sleep patterns in the EEG
Lindsley et al., (1950) lesioned the reticular formation without damaging the sensory
pathways and found continuous coma and slow wave EEG.

➢ Adametz, 1959 did experiments in which reticular formation was lesioned in multiple
surgical procedures (instead of all at once). Animals eventually reacquired normal
patterns of behavioural arousal and sleep.
 ➢ A small portion of the reticular formation in the upper pons (called the nucleus
reticularis pontis oralis) has been established as the critical area for EEG arousal.
(Magoun,1964)

➢ Fieldman and Waller (1962) lesioned out the posterior hypothalamus in cats and
animals showed no signs of behavioural arousal despite the fact that EEG continued
its normal wakefulness-sleep pattern. This study demonstrated that lesions in the
posterior hypothalamus could affect behavioural arousal patterns independently of
EEG arousal.

The current thinking is that the input from both reticular formation and posterior
hypothalamus function jointly in the maintenance of normal cycles of arousal.

CONCEPTIONS OF SLEEP

▪ The duality of sleep

▪ Temporal patterns of SWS & REM sleep
▪ REM sleep and dreaming
▪ Neural mechanisms of SWS and REM sleep
▪ Biochemistry of SWS and REM sleep
▪ Function of sleep & REM sleep

At one time it was believed that sleep in general resulted as a passive consequence of a
decline in arousal. However, the current thinking is that there are active mechanisms
controlling sleep.

The duality of sleep

Sleep considered as two separate conditions (duality of sleep). In 1950s the extensive
investigations of Nathaniel Kleitman and William Dement revealed alternating pattern of two
sleep states.

Slow Wave Sleep (SWS) REM Sleep

• Develops within 30 minutes after drifting off • Between 40 and 80 minutes after sleep
to sleep onset.
• Gradual increase in delta wave pattern (first • EEG consists of low amplitude and faster
23 minutes of sleep) waves
• By minute 17, the individual enters stage 3 • EMG level declines than observed during
and 4 SWS
• Movements of eyelids are slow and short- • EOG shows a series of rapid eye
lived movement (hence called REM Sleep)
• Muscle tension decreases to a fairly low level • Increased neural activity in Pons,
Geniculate and Occipital – areas involved
in processing visual input (“PGO
spikes”) recorded in cats.
• A comparable increase in PGO spikes in
human brain underlies the dream-like,
visual aspects that we experience during
these intervals.
 • Winkelman, Duffy and McCarley (1983)
detected on human EEG records, a small,
sudden potential that would immediately
precede an eye movement during REM
sleep. This was observed in temporal-
occipital cortical region and on the
hemisphere contralateral to the direction
of eye movement. It is possible that this
potential in humans would function in a
similar way as the PGO spike observed in
animals.

Synonymous terms for slow wave sleep (SWS) are quiet sleep, synchronized sleep, S-sleep
and NREM (no rapid eye movement) sleep.

Synonymous terms for REM sleep are active sleep, desynchronized sleep, low-voltage fast
sleep, D-sleep and paradoxical sleep.

Temporal patterns of SWS and REM sleep

• In a typical sleep pattern, a slow wave period always precedes the first period of REM
sleep. The periods of REM sleep recur every 90 to 100 minutes with generally
increasing duration of each REM sleep and decreasing amounts of stage 4.

• The duration of total sleep time and the percentage of that time spent in REM sleep
show clear changes over a lifetime.

Premature New born infant 2nd year of age Age 5 Adult

infants
75% REM sleep 50% REM sleep 30% REM sleep 20% REM sleep Total sleep time
continue to
decline slowly

• A commonly cited hypothesis to speculate about the relationship between the REM
sleep percentage and a number of species factors; Mammals who are preyed upon by
other animals exhibit generally less proportional REM sleep than do mammals who
are predators.
• Berger (1969) has shown that proportion of REM sleep can be related to the extent to
which the animal displays binocularly coordinated eye movements.

REM Sleep and Dreaming

• Dreaming was associated with periods of REM sleep (Aserinky & Kleitman, 1955
and Dement & Kleitman , 1957)
• Studies showed that:
(i) 74-80% of awakenings during REM sleep produced dream reports
 (ii) The subjective length of the dream experience correlated with the objective length
of REM sleep (3-50 minutes) episode.i.e., There is a positive correlation between the
duration of the REM sleep and description of the dream. However, when the episode
was longer than 30 minutes, the description of the dream was not much longer than 15
minutes, even though subjects would report that their dream was unusually lengthy.

Neural mechanisms of SWS and REM sleep

• Several subcortical systems are involved in the control of wakefulness and sleep.
• The diffuse thalamic system, the raphe nuclei in the pons and the anterior
hypothalamus have all been implicated in slow wave sleep.
• The locus coeruleus and gigantocellular tegmental field (FTG), both in the pons, have
been implicated in the cycling back and forth of slow wave sleep and REM sleep.

BRAIN AREA LOCATION/FUNCTION EXPERIMENTS

Diffuse Thalamic Axons of this system project to W.R.Hess (1931)

System widespread areas of the neocortex Low frequency stimulation
rather than to any specific location. of particular nuclei in the
(Set of thalamic thalamus could trigger off
nuclei) normal sleeping behaviour
in the cat, including circling
and curling.

Hypothalamus Posterior hypothalamus controls the (i) (Fieldman and Waller)

(anterior & posterior maintenance of behavioural arousal. Discussed under
hypothalamus) physiological conceptions of
wakefulness and arousal
Anterior hypothalamus & the section
of telencephalon immediately anterior (ii) Nauta (1946) lesioned
to the hypothalamus (referred to as the anterior hypothalamus in
basal forebrain area, BFA) – have the rats, finding a profound
opposite function. disturbance in sleep. For the
first 24 hours, the animals
appeared normal although
sleepless. After three days,
they fell into a coma and
died.
Dual lesions of anterior and
posterior sites in the
hypothalamus produced a
sleeping pattern, suggesting
that anterior lesion could not
compensate for the effects
of the posterior lesion.

(iii) McGinty & Sterman

(1968) lesioned the basal
forebrain area in the cat.
Then prolonged
wakefulness occurred.
 (iv) Sterman & Clemente
(1962) has found the
predicted sleeping patterns
following an electrical
stimulation of the anterior
region.

Raphe nuclei (pons) The raphe nuclei are located in both Jouvet (1969)
pons and the medulla. The nuclei When the raphe nuclei are
involved in sleep appear to be at the lesioned in cats, SWS is
pontine level. reduced roughly in relation
Control the slow wave element of to the extent of the lesion.
sleep. When more than 80% raphe
nuclei destroyed, the cats
sleep less than 15% time
and have no REM at all.
[normal pattern of cats –
approximately 50% of time
is spent in SWS and 20% in
REM sleep (Levitt,1974)]

Locus coeruleus A region of the reticular formation in Jones et al.,1977

(pons) the lower pons. When locus coeruleus is
Plays a central role in the maintenance lesioned in cats, there is a
of REM sleep. greater amount of muscle
tension than normally seen
in REM sleep; though other
features of REM sleep are
unchanged.

Gigantocellular Located near to locus coeruleus in the (i) Chase et al.,1980,1983

tegmental field pons. Monitoring intracellular
(Gigantic cells of the Role in development of REM sleep responses in FTG cells;
tegmentum, FTG) have found a depolarization
of 3-14 mV at the onset of
REM sleep.
They theorized it to be
associated with an eventual
hyperpolarization of the
alpha motor neurons in the
spinal cord.
It is possible that activation
of FTG cells result in an
inhibition of muscle tension,
typically found in REM
sleep.

(ii) Hobson, McCarley &

Wyzanski (1975)
Showed that during periods
of wakefulness, SWS and
 REM sleep, the firing rates
of neurons in the two areas
of the pons varied in direct
opposition to each other.
During REM sleep, FTG
cells were firing most
rapidly, while locus
coeruleus cells were firing
most slowly.

The Biochemistry of Slow-Wave Sleep and REM Sleep

I. Serotonin
• Found in the raphe nuclei in large quantities and acts as the critical neurotransmitter in
this region for the onset of SWS.

• Experiment I:
• Cats (Jouvet, 1969) and monkeys (Weitzman, 1969) were injected with a substance
called parachlorophenylalanine, PCPA (an inhibitor of an enzyme necessary for the
production of serotonin)
• It was expected that the animals would become insomniac. In Jouvet’s study, the
insomnia did not begin until 24 hours after PCPA injections.
• After 24 hours, insomnia was observed for about two days until the inhibiting effect
of PCPA began to wear off. After 8 days or so, the sleep pattern was essentially
normal.

• Experiment II: (Jouvet, 1969)

• An injection of 5-HTP (5- Hydroxytryptophan), the immediate precursor of serotonin
was given to PCPA treated cats.
• As predicted the insomnia suddenly was gone. It also restored SWS in cats whose
sleep had been reduced by serotonin decreasing substances other than PCPA.

• Finally Jouvet showed that the insomnia observed in cats following raphe nuclei
lesions was positively correlated with the loss of brain serotonin.

II. DSIP – delta sleep inducing peptide

• A peptide consists of 9 amino acids
• DSIP may play a role in the initiation of SWS across all mammalian species.

III. Factor S
• Contain two amino acids and found in cell walls of bacteria
• It induces EEG signs of sleep including all aspects of sleep
• It has the capability of inducing 50% increase in SWS (REM free sleep)

IV. Nor-epinephrine (NE)

• Inhibitory role in REM sleep
• Drugs that inhibit NE generally increase the incidence of REM sleep
• Drugs such as amphetamine and tricyclic antidepressants that increase brain NE
activity generally produce decreases in REM sleep.
The function of sleep

The explanation of why sleep itself occurs at all remains a great puzzle.
• Researchers have looked to possible behavioural explanations for the process of sleep.
• Sleep deprivation studies in animals found that sleep deprived animals suffered more
impairment in organ functioning and greater weight loss (despite increased food
intake)
• Webb (1971, 1975) pointed out that without sleep an animal would expend energy
during some portions of the day that would be poorly suited to survival. A period of
inactivity would allow an animal to conserve its energy stores for periods of the day
in which activity would be most valuable.
• A sleep-wake cycle has been evolved as a strategy for survival as a species.
• Although the deprivation of sleep in general or the selective deprivation of REM sleep
might be presumed to produce deleterious effects on a behavioural or physiological
level; surprisingly few effects of this kind are observed in humans. Normal sleep
patterns return after a relatively short time subsequent to sleep deprivation.

The function of REM sleep

• Early studies of REM deprivation in humans (those prior to about 1965) indicated
pronounced psychological effects: irritability, ravenous appetite, increased oral
behaviour, and oral symbolism in the subjects’ thinking.

• Kales et al., showed that following REM sleep deprivation, normal cycles of REM
sleep return after a transitory “rebound” period. [Rebound period: increased
frequency, depth and intensity of REM sleep following sleep deprivation or
significant stressors.]

• The rebound phenomenon in REM sleep deprivation studies strongly indicates that in
some way REM sleep is a necessary element of one’s sleep.

• According to Dement (1969), REM sleep serves as a “safety valve” that allows a great
deal of neural activity to occur in the brain without any behavioural consequences.

• One prominent hypothesis concerning REM sleep focuses upon the need to maintain
muscle tone for species with binocular vision. Berger (1969) emphasized the
difference in REM sleep across as well as across a lifetime. A proportionate measure
of REM sleep increases in various species as there is a decline in the percentage of
completely crossed visual nerve fibers at the optic chiasma. According to Berger, the
50% partial decussation or crossing of fibers in the human visual pathway is
associated with the greatest development of REM sleep.

DISORDERS OF AROUSAL AND SLEEP

1. ADDH (Attention Deficit Disorder with Hyperactivity)

2. Narcolepsy
3. Insomnia
4. Somnambulism
5. Enuresis
6. Night terrors
 7. Sleep apnoea
8. SIDS (sudden infant death syndrome)

CIRCADIAN RHYTHMS AND CLOCKS

• Biorhythm - Inherent timing mechanism that controls or initiates various biological

processes.

• Biorhythms are cyclic behaviour patterns of varying length displayed by animals,

plants, and even single-celled organisms. Mammals display a number of biorhythms,
including circadian (daily) rhythms and circannual (yearly) rhythms.

• Biological clock is the neural system that times behaviour.

• The activity period of most animals is about 24 hours in an environment in which the
lights go on and off with regularity. Our own sleep–wake period also is about 24
hours. This day-night rhythm is known as circadian rhythm.

• Circadian rhythm determines the variation our level of activity as well as important
physiological processes such as body temperature, hormone levels in blood, blood
pressure and heart rate.

• To determine whether a rhythm is produced by a biological clock, researchers have

designed three types of tests in which they remove relevant cues. A test can be given
(1) in continuous light or (2) continuous darkness, or (3) the selection of light or
darkness can be left to the participant. Each treatment gives a slightly different insight
into the periods of biological clocks.

• Jurgen Aschoff and Rutger Weber first demonstrated that the human sleep–waking
rhythm is governed by a biological clock (Kleitman, 1965). They allowed participants
to select their light–dark cycle and studied them in an underground bunker where no
cues signaled when day began or ended. The participants selected the periods when
their lights were on or off, when they were active, and when they slept. In short, they
selected the length of their own day and night. Measures of on-going behaviour and
recording of sleeping periods with sensors on the beds revealed that the participants
continued to show daily sleep–activity rhythms. This finding demonstrated that
humans have an endogenous biological clock that governs sleep–waking behaviour.

• Although the period of the participants’ sleep–wake cycles approximated 24 hours

before and after the test, during the test they progressively deviated from clock time.
Rather than being 24 hours, the period in the bunker ranged from about 25 to 27
hours, depending on the participant.
 • The participants were choosing to go to bed from 1 to 2 hours later every “night.”
Soon they were getting up at about the time the experimenters outside the bunker
were going to bed.

• In the absence of environmental cues, circadian rhythms are free running (rhythm of
the body’s own devising in the absence of all external cues), lasting a little more or a
little less than their usual period of about 24 hours, depending on the individual
organism or the environmental conditions.

• Endogenous rhythmicity is not the only factor that contributes to circadian periods.
There must be a mechanism for setting rhythms to correspond to environmental
events.

• Cues that reset a biological clock to a 24- hour rhythm are called Zeitgebers. When a
clock is reset by a Zeitgeber, it is said to be entrained. Normally, light is the most
potent entraining stimulus. The property that allows the biological clock to be
entrained allows the circadian rhythms to synchronize with seasonal changes in day–
night duration.

• The difference between a person’s circadian rhythm and the daylight cycle in a new
environment can produce the feeling of disorientation and fatigue called jet lag.

NEURAL CONTROL OVER CIRCADIAN RHYTHMS

• The regulation of circadian cycle is accomplished by the suprachiasmatic nuclei

(SCN) in the anterior portion of the hypothalamus, just above the optic chiasma.
• The information regarding the light conditions is received by the SCN via direct
pathway from the retina and another via lateral geniculate nucleus in the thalamus.
• Through these routes, circadian cycles can be entrained to light-dark conditions.
• Without these pathways, light-dark conditions no longer synchronize the cycle.
• The result then is a free-running cycle slightly longer or slightly shorter than 24 hours
(depending upon the species) or else reliance upon other external cues.