circadian rhythms

Sleep wake cycle-

Theres an endogenous clock which is free-running (works without external cues + lasts 24 hrs). Normally doesnt work alone e.g. daylight- can adjust to suit environment. Sleep wake cycle may be controlled by external cues.  Research suggests an internal clock as circadian rhythms persist when isolated from light.

Core body temp-

Core body temp indicates circadian rhythm. lowest-4.30am (36); highest 6.30pm (38). Slight trough after lunch (not because of eating)- afternoon siestas because of dip. Bi-daily rhythm.

Hormones-

Hormones follow circadian rhythms. cortisol low- midnight, peaks 6am. Produced in stress and aids alertness when waking (wake early, low cortisol= hard to think). Melatonin (induces sleep) and growth hormones peak midnight.

Spans less than a day.

Sleep stages-

5 stages of sleep- four NREM and one REM. One sleep cycle= all 5 stages= 90 mins.

1+2= light sleep (charactorised by change in brain activity). Awake brain produces beta waves. More relaxed?= brain waves slow and greater amplitude (alpha waves). Going to sleep?- waves slow further, greater frequency (theta waves)- accompanied with bursts of activity- inc. wave frequency (sleep spindles)and amplitude (k-complexes). 3+4= deep sleep- slower delta waves (SWS- harder to wake). Most of bodys repair work takes place- growth hormones.

REM- fast, desynchronised EEG activity resembling awake brain. Cycle continues throughout the night- SWS gets shorter, REM longer. infants cycle is 60 mins, 90 in teens.

Basic rest-activity cycle-

90 min clock also works throughout the day- basic rest-activity cycle (BRAC). Friedman and Fisher (1967) observed eating and drinking behaviour in psychiatric patients over periods of 6 hrs= detected a clear 90 min cycle.

Spans more than a day, less than a year. Doesn’t have to be monthly.

Monthly cycles-

Driven by fluctuating hormone levels. Function- regulating ovulation. Pituitary gland (controlled by hypothalamus) releases FSH (follicle stimulating hormone) and LH (luteinising hormone) which cause ovaries to ripen egg + triggers release of oestrogen. When ripe, ruptured follicle secretes progesterone causing womb lining to prepare for pregnancy (inc. blood supply). After two weeks of ovulation + no pregnancy, progesterone levels reduce and lining of womb sheds.

Monthly rhythms in males- Empson (1977) studied 21 males body temp and alertness over periods varying from 49-102 days. Found periodic variation of body temp and morning alertness within a cycle of 20 days.

Seasonal affective disorder (SAD)-

Depression during winter and recover in summer. Sufferers have severe symptoms due to inc. darkness (lower mood). Research shows melatonin and serotonin are secreted in the dark (by pineal gland). More dark= more melatonin= less serotonin (melatonin produced from serotonin). Low levels of serotonin associated with depression.

Suprachiasmatic nucleus (SCN)-

Main endogenous pacemaker. A cluster of nerve cells that lie in the hypothalamus. Located above optic chiasm (where optic nerves from eyes cross). SCN obtains information about light from eyes. Also occurs when eyes are shut- light penetrates eyelids. If endogenous clocks slow, light automatically shifts ahead to stay in sync with world. SCN is a pair of structures (one in each hemisphere of the brain- ventral and dorsal) ventral is quickly reset by external cues, but dorsal is less affected by light= resistant to reset (Albus, 2005).

SCN sends signals to pineal gland to inc. melatonin production at night (induces sleep + inhibits brain mechanisms which promote wakefulness). In birds and reptiles pineal gland is beneath skull- directly regulated by light (light inhibits melatonin production) e.g. lizards have 3^rd eye.

Light-

Dominant zeitgeber in humans. Light can reset SCN and other oscillators in the body as protein cryptochrome (CRY) is light sensitive. Campbell and Murphy (1998)- shined light on back of pp’s knees and shifted circadian rhythms.

Temp-

Cold-blooded animals- variation of external temp affects circ. rhythm- cold temps= reduced activity, warm= activity (sleep-wake). Research in warm blooded animals suggests daily changes in body temp have own circadian clock + these changes entrain other circ. rhythms (Buhr, 2010).

Social cues- 

Scientists thought cues were main zeitgebers for circadian rhythms as eat and sleep at socially determined times. Now- know light is dominant but not all oscillators are reset primarily by light e.g. liver + heart cells reset by eating (Davidson, 2006)

Bio. rhythms driven by endogenous pacemakers. Some desynchronise.

Shift work-

Night workers required to be alert= sleep during day (against nat. rhythm + zeitgeber cues). Exp. circ. 'trough'  of dec. alertness in shifts at midnight- cortisol lowest + 4am body temps lowest (Boivin, 96). Those sleep by day exp. sleep problems (light + interruptions)= reduces sleep quality. Daytime sleep= 1/2hrs shorter than night; REM affected (Tilley + Wilkinson,82). Poor quality= harder stay awake in trough. Knutsson (86) found- shift workers of 15+ yrs X3 likely develop heart disease. Martino (2008) linked shift work + organ disease- may be direct effect of desynchronisation or indirect e.g. sleep disruption.

Jet Lag-

Physiological effects of disrupted circ. rhythms. Bio. rhythms can't cope with sudden/ large changes (dorsal SCN= several cycles to resynchronise time changes). Winter (2008)- 1 day per hr change. Jet lag symptoms= appetite loss, nausea, fatigue, disorientation, insomnia, depression. Demonstrate jet lag effects?= study US major league baseball teams. Recht (95) analysed results over 3 yrs. Teams= east-west (phase delay= easier adjust e.g. sleep later) won 44% games + W-E(phase advance- harder e.g. get up early) won 37% (W 3hrs behind E).

Infancy-   Need more sleep (16hrs). Different sleep patterns and stages (not continuous- wake every hr- cycle shorter than 90mins). Have quiet + active sleep (immature SWS and REM). 1/2 infancy sleep is active. Early infants- light sleep then (after 20mins) gradual deep sleep (adults quickly into deep). By 6mths circ. rhythms established (main sleep cycle) + at 1 mainly night with 1/2 naps. Deep sleep periods lengthen and dec. active/REM sleep. Can't be sure REM is accompanied with dreaming- no reports.

Childhood-   By 5, have EEG patterns similar to adults. Sleep more (12hrs) + more REM activity (30% total sleep). Boys sleep more. Parasomnias common e.g. sleep walking + night terrors.

Adolescence-   Childhood- need for sleep dec. Adolescence incs to 9/10hrs. Circ. rhythms change to feel more awake later and difficulty getting up (phase delay). In REM males may ****** or ejaculate.

Adulthood and old age-   Normally 8hrs. 25% REM. Parasomnias rare but inc. sleep disorders e.g. insomnia and apnoea. Inc. age- total sleep same but have trouble getting to sleep and wake up frequently (up to X6). Sometimes nap to satisfy sleep needs. Sleep patterns change- REM dec. (20% total sleep) and SWS (5% or less). NREM inc. Older people exp. phase advance (sleepy early, wake early).

Two sleep stages- slow wave sleep (SWS) and REM sleep. Oswald (80)- different functions- SWS=body repair. REM= brain recovery.

SWS-

Growth hormone secreted in SWS stimulates growth. Important in child + adulthood- enables protein synthesis, cell growth (restoration body tissue- cells constantly need renewing)= bodys natural recovery process. GH secreted in pulses during day but mainly released night during SWS. Sassin (69)- sleep cycles reversed 12hrs- GH release also reversed (shows GH release controlled by neural mechanisms in SWS). Van Cauter + Plat (96)- amount of GH released correlates with amount SWS. Van Cauter (2000)- decline of GH in old age associated reduced SWS.

Immune system-

Krueger (85)- lack of SWS associated with reduced immune system functioning (bodys defence-consists of antibodies which are regenerated in cell growth + protein synthesis in SWS.

Brain Growth-

Suggested amount of REM sleep proportional to offspring immaturity (babies more than adults) e.g. platypus immature at birth= 8hrs REM per day; dolphins (can swim at birth)= almost no REM sleep (Siegel, 2003). Shows relationship between neural development + REM.

Neurotransmitters-

Activity may be affected by REM sleep. Siegel + Rogawski (88)- REM allows for breaks in neurotransmitter release= for neurons to regain sensitivity + proper body functioning. Support from anti-depressants e.g. MAOI's aim to inc. monoamine neurotransmitter levels (i.e. serotonin + dopamine). MAOI's may eradicate REM (inc. monoamines- receptors don't have to be revitalised= no need for REM sleep).

REM + Memory-

Crick + Mitchinson (83)- in REM unwanted memories discarded= important memories accessible. New research suggests complex relationship between memory and sleep (Stickgold, 2005)= REM important in consolidation of procedural memory (skills) + SWS sleep important for consolidation of semantic (knowledge + meaning) and episodic (events) memory.

Energy Conservation-  Warm blood animals need use alot energy= maintain constant body temp- harder for small animals with high metabolic rates (chemical processes in body) e.g. mice. Activities use energy + animals high metabolic rate use more. Sleep provides period of enforced inactivity (use less energy) e.g. hibernation- means conserving energy. Webb (1982)- hibernation theory.

Foraging Requirements-  Sleep=necessity. Constrained by food requirements- gathering. Herbivores spend time eating food poor in nutrients= eat alot + can't afford spend time sleeping. Carnivores eat food high in nutrients= don't need continuously eat= can sleep (conserve energy).

Predator Avoidance-  Sleep constrained by predator risk. Predator- can sleep longer. Prey- sleep less= remain awake= avoid predators. Logically- prey shouldn't sleep- vital = best sleep when least vulnerable.

Waste of Time-  Meddis (1975)- waste of time hyp= sleep helps animals avoid predators when vulnerable. Most= during dark hrs + in hidden places= sleep ensures stillness when nothing to do. Siegel (2008)- awakes riskier than sleep= chances of injury inc. What know of sleep patterns- enables energy conservation + avoids danger e.g. brown bat awake when need be (when insects awake).

Primary insomnia= sleep problems not associated other condition/ cause. 2ndary= underlying cause.

Genetics-

May be genetic vulnerabilty to insomnia. If genetic= likely pass from parent- child= many insomniacs. Beaulieu-Bonneau (2007)- 34.9% insomniac surveyed said had 1st degree relative with current/ history of insomnia.

Hyper arousal-

Insomniacs exp. higher levels physiological arousal than non-sufferers. Primary insomnia usually associated with inc. body temp, heart rate + metabolic rate. High arousal levels in day= insomniacs feel less sleepy than normally + continued arousal= difficulty sleeping.

Brain chemistry-

Insomnia may be caused by change brain chemistry. Winkelman (2008)- people with insomnia for 6mnths= lower levels of GABA (inhibituary neurotransmitter- dec. brain activity). If have less GABA, brain not being quietened at night= not able to switch off to sleep.

Sudden, uncontrollable attacks of sleep- Lehrman + Weiss (43)- disguises sexual fantasies. 

REM-

Classic symptom= loss muscle tone ('cataplexy'). Similar happens REM sleep. During day exp. intrusions REM-type sleep (hallucinations). Night= normal REM. 60's= malfunction of system regulates REM.

HLA-

80's= research- narcolepsy linked mutation of immune system. Honda (83)- inc. frequency of type 1 HLA (human leukocyte antigen) in narcoleptics= molecules on surface white blood cells + coordinate immune response. Recently- 90%+ narcoleptics with cataplexy have HLADQB1*0602 (stanford medical centre, 2012). Not clear how lead to narcolepsy.

Hypocretin-

Uncovered link- neurotransmitter hypocretin + narcolepsy. Regulates sleep + wake through interactions with systems ( that regulate emotion + homeostasis in hypothalamus (Sakurai, 2007). Normally 10-20,000 hypocretin producing cells in hypothalamus- narcoleptics= low lvls.

Incomplete Arousal-

Sleep walking= arousal disorder- person partially awake (engaged in activities associated with awake but asleep). Deep sleep (SWS)= difficult to rouse. Brain activity recordings from sleep walking- show mixture delta (typical SWS) + high freq. beta waves (charactoristic of awake). Sleep walk when deep sleep awakened but brain arousal incomplete.

Risk Factors-

Some factors inc. likelihood sleep walking e.g. sleep deprivation, fever, stress, psychiatric conditions (Plazzi, 2005). Hormone changes in puberty + menstruation can trigger sleep walk. Only in some people triggered= inherited vulnerability.

Genetic Basis-

Evidence- sleep walk may be inherited. Broughton (1968) found prevailance to sleep walk in 1st degree relatives (e.g. siblings, parents + children)= 10X greater than in general population.