sleep and circadian rhythms

circadian rhythms

rhythms for regular patterns of activity associated with a 24h cycle

endogenous cycles

our brain and body spontaneously generate their own rhythms based on the earths rotations. these can also be annual or seasonal.

human circadian rhythms

controls sleep, eating and drinking, body temp, hormone secretion, urination, drug sensitivity and performance in neuropsychological tests.

early discoveries in humans

no light cues, ppts selected own light-dark cycle, 25-27h cycle. humans have an endogenous biological clock which governs sleep-wake behaviour

purpose of rhythms

keep internal workings in phase with outside world. work alongside external cues

zeitgebers

external cues that serve to set our biological clock e.g. light, activity, meals, temp, tides). they can entrain biorhythms

seasonal affective disorder

low light levels in winter are not enough to entrain circadian rhythms. phase-delayed sleep and temp rhythms. can be reset by exposure to bright light (phototherapy)

jet lag

mismatch of internal circadian clock and external time. travelling west → phase delays. travelling east → phase advances. brains bio clock resets faster than organs.

shift workers

• often fail to adjust completely

• tend to have more accidents

• increased vulnerability to disease

chronotypes

cycles differ between people, and can lead to different patterns of wakefulness. rhythms show similar patterns in other species.

what effects chronotypes

genes, environmental factors, age, culture

patterns of chronotypes

morning people in infancy, childhood, adulthood and old age. shift towards evening preferences in adolescence

• this can lead to social jet lag, and create issues in school (which starts early)

1st evidence for neurological basis of bio clock

Richter → wild rats showed activity in the dark, and inactive in the light. he performed electrical lesions to locate bio clock. rats lost rhythmic behaviour after lesions to hypothalamus.

suprachiasmatic nucleus

~50,000 neurons in humans.

it generate circadian rhythms in a genetically controlled manner. neurons more active in light than dark. a single extracted cell continues to produce APs in rhythmic pattern. SCN transplantations show recipient experiencing donors rhythm

how does light reach SCN

retinohypothalamic tract, formed by photosensitive retinal ganglion cells. these cells have their own photopigment called melanopsin, and can respond directly to light.

structure of SCN

core (ventral) and shell (dorsal). retinohypothalamic tract activates core cell which entrain shell neurons (which consists of M cells for morning light and E cells for evening light)

other SCN inputs

non-photic information. from Raphe Nucleus and intergeniculate leaflet of thalamus. informs SCN about eating, movement etc. so doing these things at night impacts sleep cycle.

how does SCN work

drosophila - per gene and PER protein. PER builds up overnight and is being broken down during day.

tim gene and TIM protein. when TIM and PER combine they shut down per gene.

how SCN entrains slave oscillators

• projections to nuclei in hypothalamus and thalamus, which then project to other areas

• projections to pituitary gland to control hormone release and affect various organs in the body

• indirect messages to autonomic neurons in the spinal cord to inhibit pituitary gland

SCN influence on sympathetic NS

arousal, mobilisation of glucose and glucocortoid secretion by adrenal glands

SCN influence on parasympathetic NS

relaxation, digestion, melatonin secretion by pineal gland

further effects of SCN

• breeding of animals (melatonin production changes based on light, days get shorter in winter)

• cognitive and emotional behaviours (e.g. fear heightened at night)

• attention and memory (affected by time of day)

• treatment of disease (e.g. higher likelihood of stroke/heart attack in morning)

sleep

a natural periodic state, reduced response to environmental stimuli and decreased mobility. in all cultures and most species

homeostatic control of sleep

if we do not sleep enough, we accumulate sleep debt, and we will make up for the lost sleep the next time we fall asleep

circadian control of sleep

sleep tends to happen in a particular time during the 24h cycle

subjective measures of studying sleep

• asking people

• scales and questionnaires

• sleep diaries

objective measures of sleep

• actigraphy → watches that record activity, like duration and quality of sleep

• polysomnography → EEG, EOG and EMG recordings, measure sleep stages

brain activity during wakefulness

alpha activity → regular med freq waves. recorded at rest, mostly when eyes are closed

beta waves → irregular higher freq waves. recorded when alert and processing information

brain activity during sleep

five sleep stages

stage one

3.5-7.5Hz, presence of theta activity, the transition between sleep and wake

stage two

12-14Hz, sleep begins, characterised by sleep spindles and the K complexes

stage three and four

>3.5Hz, high amplitude and low freq delta activity. distinction between these stages is not clear-cut. stage 3 contains 20-50% delta activity whereas stage 4 contains <50%. these stages are collectively referred to as slow-wave sleep (deep sleep)

stage five

REM sleep. characterised by increase brain activity and muscle atonia. deep sleep in terms of muscle activity, but light sleep in terms of increased brain activity. where most dreams occur

sleep cycle

• when we fall asleep, we progress through stages 1-4 in a sequential order

• after ~1h, begins to cycle back from 4-2 then REM

• sequence repeats, with each cycle lasting ~90mins

dreams

considered important in psychoanalysis. mostly are related to events in a persons life. >64% associated with sadness, anxiety or anger

activation-synthesis hypothesis

• brainstem activated during REM, and sends signals to the cortex which creates images with actions and emotions from memory

• less active frontal cortex, so no logic in timing or sequence of events

coping hypothesis

• dreams are biologically adaptive, enhanced coping strategies

• dream abt threatening events and emotional challenges to overcome problems

neural basis of sleep

melatonin → secreted during dark, promotes sleepiness

adenosine → accumulates during day after prolonged wakefulness, promotes sleep

caffeine → antagonises effects of adenosine

brain inhibition during sleep

GABA- inhibitory NT released by neurons in preoptic area of hypothalamus, ventro-lateral part, inhibits arousal centres and promotes sleep. damage to this area causes insomnia

neural basis of wakefulness

reticular formation in brainstem extends from medulla to forebrain and promotes arousal. stimulation wakes up a sleeping cat.

NTs for wakefulness

Ach → stimulates neurons leading to wakefulness

5HT → promotes wakefulness when animal is moving

norepinephrine → increases activity in various cortex areas

orexin → maintenance of wakefulness

histamine → widespread excitatory effects