S2W7Sleeppt2 Flashcards
zeitgebers
Signals from the environment that control body clock e.g. light
Roenneberg, Kumar & Merrow (2007) importance of light
When under no obligation to rise at a particular time, people on the eastern edge of Germany wake 30mins earlier than those on the west, consistent with 30min difference in sun.
Less pronounced the larger the city. Large cities have less natural light.
Age preferred bed time peaks
20
Biss & Hasher (2012) night owls
Lead to ‘social jet lag’:
Lower grades (despite average, or above-average intelligence)
Increased alcohol use and overeating
Less happy overall
Circadian clocks
Contained in cells.
Collections of genes which regulate the switching on of other genes critical for cell physiology and metabolism.
Nearly half of all mammalian genes expressed rhythmically.
Have been directly implicated in sleep disorders, diabetes, cancer and bipolar disorder.
Suprachiasmatic Nucleus (SCN)
Synchronises circadian clocks
Part of hypothalamus.
SCN neurons have direct input from retina to synchronise day/night cycle.
Mechanisms which allow them to remain synchronised to each other even in constant darkness.
Generate a circadian rhythm of firing frequency that allows them to synchronise other cells.
Retinohypothalamic path
Light resets SCN via branch of the optic nerve known as retinohypothalamic path.
Travels directly from the retina to SCN.
Comes from a population of ganglion cells that have own photopigment called melanopsin.
Cells respond to light and do not require input from rods/cones.
Damage to SCN
SCN entrains to 24hr cycle, and synchronises other peripheral circadian clocks.
Damage to SCN causes the peripheral clocks to lose rhythmicity.
Damage to SCN
Welsh, Takahashi & Kay (2010)
SCN cells from mouse, fused with enzyme from firefly.
Each time neuron fires the enzyme releases a photon.
Photonm frequency recorded showed distinct daily circadian rhythms.
However:
SCN provides more precise rhythm than neurons independently.
Relationships between neurons alter rhythms at whole animal level, accounting for seasonal changes in day length.
Genes
Light triggers sequence of processes in SCN neurons, leading to expression of the circadian clock-genes.
Two types of genes responsible for circadian rhythm in fruit flies:
Period genes - produce protein PER
Timeless genes - produce protein TIM
PER and TIM
Promote sleep
Synthesis of PER and TIM low at sunrise (shown by high mRNA levels)
Followed by increase in proteins themselves – PER and TIM high at night.
Increased levels of PER and TIM lead to decline in mRNA (which then inhibits protein synthesis).
Melatonin
SCN regulates pineal gland, (endocrine gland posterior to thalamus).
Pineal gland secretes melatonin, hormone that increases sleepiness.
Secretion begins 2-3 hours before bedtime.
Production highest at night.
Resets biological clock through effects on SCN receptors.
Melatonin taken in afternoon used as sleep aid.
Circadian rhythm sleep disorders
Advanced sleep phase disorder (ASPD)
Delayed sleep phase disorder (DSPD)
Irregular sleep-wake disorder (ISWD)
Familial advanced sleep phase disorder (FASPD)
Utah family mid 1990s.
Sleep phase was advanced 4-6 hours.
Put in isolation for 3 weeks.
Showed 1 hour shortening in circadian period.
Mutation in Per2 gene identified, and mice carrying this mutation were created.
Mice showed 4-6 hour advancement too..
Familial natural short sleepers (FNSS)
Mutation in DEC2 gene.
Family needed only 6 hrs sleep/day
Replicated in GM mice.
Narcolepsy (Non-circadian rhythm)
1/1000 people.
Clear genetic component.
90% carry HLA-DR2/DQ1 gene.
Symptoms interpreted as an intrusion of an REM-like state into wakefulness:
- Sleepiness during the day
- Occasional cataplexy
- Sleep paralysis
- Hypnogogic hallucinations
Narcolepsy causes
Lack hypothalamic cells that produce/release orexin.
Found in Huntington’s Disease (loss of neurons in hypothalamus: difficulty staying asleep/awake)
Orexin cannot be administered to sufferers as it cannot cross the blood-brain barrier.
Narcolepsy treated with stimulants (Ritalin).
REM Behaviour Disorder (RBD)
Most people’s postural muscles inactive during sleep.
Move violently and injure self/others.
Caused by inadequate inhibitory transmission (e.g. deficient GABA).
Mice deficient in GABA show running, jerking in REM.
Reflect acting out of dreams
Associated with Parkinson’s
RBD brain causes
RBD and REM manifestations of brainstem-generated twitching of skeletal muscles.
Congenitally blind people exhibit REM despite having no visual dream content.
Cats with lesions to the visual cortex continue to exhibit REM (they shouldn’t).
Stimulation of brainstem can induce complex behaviours of an evolutionary nature (fight-or-flight).
Sleep walking
Complex movements carried out during sleep.
During NREM sleep
Could not occur during REM due to muscle atonia.
Causes unknown.
Runs in families occurs mainly in children.
Risk factors: sleep deprivation, stress, alcohol.
Violence during sleep
Prevalence of sleep-related violence is 2%.
RBD episodes more likely to lead to spousal injury during dreamed attack.
Inadvertent murder or suicide is associated with sleepwalking rather than RBD.
Sleep deprivation Randy Gardner
Stayed awake for 11 days in 1964 for a high school science fair.
Experienced disorganised speech, delusions and paranoia.
Case study – Peter Tripp
Radio wake-athon for charity (200 hours)
Supervised by researcher:
Drop in body temperature
Lower the temperature the crazier he got:
Hallucinating
Lost hold on reality
5th day hearing voices
When we sleep we enter REM every 90 mins
He was awake but entered REM dreaming (hallucinating)
Abusing people.
Long term: change in personality, relationship problems…
Shao et al. (2014)
Effects of sleep deprivation on brain
36-hours SD.
Reduction in functional connectivity between amygdala and executive control and inhibition regions (prefrontal cortex, ACC) .
Underlies difficulties in emotional regulation in SD
SD explicit learning and memory problems
Effects of SD on hippocampus.
SD prior to learning inhibits hippocampal-dependent encoding (less effective at encoding the information).
SD following learning inhibits hippocampal-dependent consolidation (fail to consolidate the material).
Inhibits neurogenesis (growth of new neurons) and long-term potentiation.
Chronic SD leads to shrinkage of hippocampus
.
4 hours per day for month: 10% smaller hippocampi in rats.
SD working memory, and attention problems
Problems with:
Verbal fluency, non-verbal planning, creativity
Team planning exercises
Attention and Working Memory (different part of brain to explicit)
WM deficits accompanied by decrease in activity in prefrontal cortex, thalamus and posterior parietal cortex.
