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Sleep and biological rhythms (Biological basis of circadian rythyms (4 key…
Sleep and biological rhythms
Homeostatic regulation of sleep
hypnotoxin (sleep toxin) theory of sleep
builds up during wakefullness and decreases during sleep
now identified as adenosine
breakdown product of ATP (energy battery)
4 receptors in humans (A1, A2a, A2b, A3)
A1 and A2a present in brain
caffeine is an adenosine receptor antagonist
broken down by adenosine deaminase
can have genetically variables amounts and quick or slow acting forms
Not the sole cause of process S
adenosine receptors in parts of brain responsible for wakefulness
dynamics of adenosine build up not completely exponential
extreme activity leads to larger amounts of adenosine but doesn't increase SWS amount
Other factors
cytokines
interferon alpha, interleukin and tumour necrosis factor all shown to induce sleep
other sleep/immune factors
cholecystokinin, arginine vasotocin, vasoactive intestinal
peptide, growth hormone-releasing hormone (GHRH),
somatostatin, prostaglandin D
Biological basis of circadian rythyms
4 key properties
persist without time cues
phase can be shifted by light/drugs
period can be entrained (can't change time period too much)
clock does not change with temp.
Suprachiasmatic Nucleus
contains biological clock
SCN lesions disrupt circ. rhythms
SCN cells do not require direct neural connections to act but can use chemical input
each individual cell has own biological clock
cells inhibit themselves when too much of proteins (per and tim) has been produced
SCN inputs
melanopsin containing retina cells
detect light, transmit message to SCN
Intergeniculate leaflet of the lateral geniculate thalamic nucleus
pathway for other external input to affected biological clock
eg food
Melatonin
secreted by pineal gland
occurs when it is dark after receiving input from SCN
slight hypnotic effect
taken medicinally to help shift circadian rhythm, not super effective, much more effective to get light
Independence of process C and S
evidence for
circadian oscillator can be shifted without affecting SWS
during a forced desyncrony protocol the two processes are separated
isolated from time givers and constant dim light
gradually pushing back sleep phase
sleep period gets further and further away from bodies own biological rhythm
Sleep that occurs during normal wake period following sleep deprivation is still associated with sleep rebound
daytime naps have expected amount of SWS relative to amount of time being awake
animals with lesions in circadian pacemaker show homeostatic not circadian properties
evidence against
in forced desynchrony protocol there is a slight interaction between circ and hom
circadian phase does slightly alter SWS
sleep deprivation reduces phase setting ability of light