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Chapter 11

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Michael Inzlicht

Chapter 11: *Trent Uni has done a lot of research on sleep Circadian Rhythms • light helps entrain (= reset) our clock to 24 hours o a longer free-running cycle is why we have an easier time adjusting to phase- delay • ultraradian = rhythms shorter than 24 hrs = (high-low alertness cycle of 90-120 mins) • infradian = rhythms longer than 24 hrs Variations in Sleep Patterns • melatonin drops dramatically at the onset of puberty, so most adolescents are nightowls o teens tend to have delayed sleep phase syndrome = we like to sleep in more • night shift workers more likely to get breast cancer, accidents, make significant errors • daylights saving time was created to save energy during world war I Internal Clocks • SCN = suprachiasmatic nucleus= our internal master clock/circadian oscillator, in the hypothal o Above optic chiasm (axons of RGC cells, known as NIF=non-image-forming cells, leave the optic nerve and project to the SCN, forming the retinohypothalamic pathway) o Unlike other RGC, NIF do not process visual info. contain photopigment melanopsin o Active only during the day, Regardless of whether species is diurnal or nocturnal o Transplanting SCN tissue causes the recipient to be like the donor’s cycle • Clocks in other tissue (peripheral clocks), particularly the liver, adjust slowly to light/dark o These are more influenced by daily feeding cycles o So, a good way to beat jet lag is to immediately adjust mealtimes to current time zone Cellular Basis of Circadian Rhythms • protein production + degradation requires 24hrs: genes are per (period), tim (timeless), Clock (Circadian Locomotor Output Cycles Kaput) that each code for proteins o Tim and per proteins inhibit the Clock protein o Clock protein promotes prod of tim and per, though • Per,tim LOW morn, activates clock  per, tim RISE during afternoon and peak in eveninginhbits clock so DOWN per tim  per tim DOWN during night Biochem and Circadian Rhythms • SCN regulates and responds to melatonin (= an indoleamine secreted by pineal gland) o Melatonin is low during the day and rises in hours before sleep, peaking at 4am and suppressed by light, mainly bright lights. Produces a phase advance, helps jet lag  Giving melatonin at night will have no effect but day has a sedative effect  High BMI, smoking  LOW melatonin • Cortisol is high in morning, low at night o Levels build as we’re sleeping and are highest when we first wake up • Breast cancer linked to exposure to artificial light, melatonin suppresses estrogen synth • 2pm-8pm is where we’re most awake/aware • Body temp lowest when asleep SAD = Seasonal Affective Disorder • Greater than normal serotonin decrease in winter, Disruptions in melatonin release • Treated with UV bright light exposure, with or without melatonin + antidepressants o Light therapy at dawn corrects people who stay up too late o Light therapy in evening helps people who sleep too early • Icelanders do not experience SAD despite the cold/high latitude, Maybe protective genes Stages of Wakefulness and Sleep • Desynchronous brain activity is linked to relatively independent action of many neurons, correlated with alertness. And synchronous is when they fire in unison, i.e. deep sleep • Wakefulness= alternating alpha (= awake but relaxed, 9-12 Hz, larger amplitude, more regular than beta).beta (= thinking + very alert, 15-20 Hz, irregular, low amplitude) wave patterns • Stage 1 = 10-15mins = theta (4-7 Hz), heart rate + muscle tension begins to decrease, similar to EEG of a beyond drowsy, muscle jerk (myoclonia), falling dream • Stage 2 = 15 mins = theta + sleep spindles = short bursts of 12-14Hz, generated by thalamus-cortex interactions, can happen in other stages of NREM. K-complex = burst only in Stage 2, spontaneously or in response to unexpected stimuli. might reflect brain trying to keep us asleep while monitoring external world. Stage 2 accounts for half of the night’s entire sleep. • Stage 3 + 4 = 1 hour = Delta = 1-4Hz very low activity, parasymp NS. Some delta in Stage 3 and Stage 4 (about 50%) consists of delta waves and awaking is difficult + disorienting. o High growth hormone secretion, GH(Growth Hormone)= also maintains immune sys, Peaks around onset of puberty, drops by 21 o Large event-related sensory-evoked potentials • forebrain metabolic activity is reduced during NREM o Metabolism rates are positively correlated with prod of free radicals • After about 90 mins of NREM, the first REM period occurs = beta with occasional theta, active sympathetic NS, heart rate, bp, breath become rapid/irregular, increased blood flow to genitals, sleep paralysis but some smaller muscles like fingers might twitch + eye + middle ear + vitals o low growth hormone secretion o reduced event-related sensory-evoked potentials • Transition between S4 and REM is rather abrupt, but usually brief passages through Stage 3 + 2 • Subsequent periods of REM continue the ultradian cycles, occurring at approx 90 min intervals • REM periods become significantly more lengthy as the night goes on, with Stages 3 and 4 being infrequent and REM dominating through hours 5-8 of a typical 8 hour sleep • PGO spikes during REM correspond to eye movements (originates in P = pontine r.f., travels to G = LGN/visual center of thalamus, and then O = occipital cortex) Sleep Throughout the Life Span • Newborns: 14-16 hrs per day asleep, half of that is REM (bc role in brain dev), Premature babies more time in REM • Adolescence and adulthood = 20% of sleep = REM, and a substantial decrease in deep sleep too • 1 year  13 hrs per day, 1-5 yrs  9 hrs, 3-6 yrs  Amount of delta (stages 3-4) is highest • Aprox age 50, total sleep decrease by about 27mins/decade. also increased awakening + decreased sleep spindles. Drops in sex hormones may be responsible, ex. Menopause o Estrogen, progesterone receptors in SCN • As we age, NREM sleep continues to decline. REM sleep stays pretty stable though Dreaming During REM and NREM • 1950s  learned wake people in REM = they can describe their dreams better • Most dreams appear to be rather ordinary (familiar places, routine activities) • We participate as characters in our dreams only about 15% of the time and imaginary strangers are more likely to appear than familiar people • Hobson + McCarley’s activation-synthesis theory of dreaming = content of dreams reflects ongoing neural activity (Ex. Being sprinkled with water  water-related dream) • Crick + Mitchison’s computerized neural network = brain forget irrelevant + unnecessary info • Winson’s evolutionary model = integrate sensory experience during REM, consolidation • Threat Simulation Hypothesis = simulate escape from threatening situations • 70% of our dreams have negative emotional content • Nightmares first appear between 3-6yrs, Decrease in frequency as puberty approaches • night terrors = occur in NREM, not REM like nightmares do. Typically within 4 hrs of bedtime, wake up disoriented/confused, not easily consoled by caregivers and might not be aware of their presence, no memory of events unless fully awaked, rapid return to sleep o 1-4% of children will experience a night terror, usually between 4-12 y.o, more boys o Abrupt scream,sweating,single-img “dreams”,pressure on c
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