PSYC 444.pdf

SLEEP MECHANISMS AND BEHAVIOR Syllabus info: 3 parts to course Neuroscience of sleep Consciousness and sleep (dreams/parasomnias) Abnormalities and sleep MANDATORY READINGS through McGill Library, use VPN if access denied, use scholar gpt, jstor, google scholar, pubme...

SLEEP MECHANISMS AND BEHAVIOR Syllabus info: 3 parts to course Neuroscience of sleep Consciousness and sleep (dreams/parasomnias) Abnormalities and sleep MANDATORY READINGS through McGill Library, use VPN if access denied, use scholar gpt, jstor, google scholar, pubmed (READINGS ARE IN EXAMS)-> principles and practices of sleep medicine Midterms: different rooms, exclusively mc questions, non cumulative (midterms are on TUESDAYS) Final: take home essay, cumulative -> test synthesis, cohesiveness, integrative (neuroscience, psychology, cognitive science) 5 essay questions (1 chosen and 1 choice out of remaining 4) Project: group project, ~5 ppl, science communication -> interaction with scientists/research/short video explaining the brain/sleep, be creative but it has to MAKE SENSE, do research, synthesize it and make it into a story/hook/provocative, holistic eval. Make it flow, look at guidelines, delegate tasks, 10 mins max, write script out beforehand, audience = uni student, intelligent adult (has to be about sleep, psychology, neuroscience), ADD CITATIONS/REFERENCES-> PHILOSOPHY TO INCORPORATE IDEA: VOULEZ VOUS COUCHER AVEC MOI CE SOIR, SLEEPING WITH A PARTNER VS ALONE, EMOTIONALITY, WELLBEING LECTURE 1: What is sleep? - Breathing, cognitive inactivity with physical inactivity, closed eyes, mobile, not conscious of environment, lying down/sitting, unresponsive, alive but not quite there - Behavioral view: INACTIVITY - Sleep scientist: polysomnographic = eeg/lie detector/graphing stages of sleep markers/brain states (cuz what if i'm pretending to sleep) - Subjective experience: feeling (body tired,sleepy), dreaming, parasomnias Dynamic balance: homeostasis (mechanistic/cognitive view), pressures of environment vs personal needs (too much or not enough sleep)-> system is CHANGING/ADAPTING Rich cognitive life: sleep is NOT state of oblivion (it is rich in cognitive life), NOT offline cognition Sleep is biological and behavioral -> to respond to sleep pressures, changes and niches (seasonal, menstrual changes to sleep) Brain hacks: neuroscientists Father of sleep research: william dement NO ONE GOOD THEORY OF SLEEP Many complementary views All living things with a nervous system have smt like sleep; sleep is ubiquitous Homeostatic theory: basic organismic activity theory Cognitive theory: memory, emotions, synaptic reorganization Sleep and consciousness: different definitions from different researchers, conscious of WHAT, not environment but SELF YES 3 states of consciousness - Wake; u can decide what to think abt and pay attention to - Deep sleep; slow/no reflexes, you forget what u were thinking abt - Rem sleep; (lucid) dreams/conscious experiences, slow reflexes, intentional and spontaneous activity (construed as reflections, plans, controlled dreams) Levels of consciousness/taxonomy 2 defining dimensional spaces: awareness/consciousness and vigilance/arousal/reactivity/alertness You descend into deeper stages of sleep, slow reflexes/low responsivity Normal human sleep DEFINITION: reversible, not reacting to world, perceptual disengagement (if u look like ur asleep u are) Contemporary view of sleep: active and dynamic process, many functions depend on SLEEP Historically: soul travel, oblivion, mini death History of sleep research: empedocles&parmenides: U need to cool down/thermoregulation, energy expenditure Plato: stable memories, vision, stabilize motions/synaptic growth with neuroplasticity Aristotle: seizure due to food gasses rising to brain (to cool brain we sleep) Hypnotoxin theory (legendre and Pieron): sleep to wash out toxins Blood from sleep deprived dogs transfused into non sleep deprived made them sleepy, turns out there is a molecule that accumulates throughout the day and disappears when you sleep Sleep is intermediary between wakefulness and death but we are vulnerable, so MUST HAVE A FUNCTION Biological rhythms, jean jacques d’ortous de mairan: heliotropic plants with relation to sun behaved same way without sun exposure (open-close leaves cycle), endogenous/inbuilt sleep rhythms EEG: 1930s, baby science Sleep science: 1970s, labs Rem sleep, aserinsky & kleitman: rem in kids, ocular reflexes experiment and left eeg on and discovered it by accident, replicated it and DISCOVERY-> rem = dreaming, sleep: dream sleep but u can dream at any stage of sleep LECTURE 2: Research methods and sleep: Subjective (retrospective/past/history/has bias but still significant if a problem is present vs prospective/present-future) vs objective estimates/measures-> outside observer’s perspective, more consensus (PSG-> electrical measures of sleep, measure physical activity) When participants are asked to keep a dream diary-> they remember more dreams (the demand, expectation plays a role-> changes the experience) You can’t do sleep the way you can track cals or exercise “sleep is always in the past” PSQI: typical questionnaire, retrospective Chronotype: morning vs night person (caveat with questionnaires: how many hours did you sleep last NIGHT (some ppl prefer sleeping during the day, doesnt capture the variability) Actigraphy: accelerometer tells you when you’re moving vs not (motor activity) added light sensors to ENSURE that we are measuring sleep and not immobility, often used in geriatric research, cheap Ideal nap time; set alarm for 23 mins? U dont want to enter delta sleep because cycle is 90 mins long Temp regulation: Temp dips at 3-4 am (u feel cold) then temp starts rising Sleep is behaviorally active (thermoregulation, mental activity) Brain imaging during sleep: low temporal resolution, uncomfy, expensive FNIS/NIRS is better Portable eeg/peripheral devices: muse (meditation), dreem, oura ring (HR variability) Spatial resolution (where in the brain), temporal resolution (when, granular and time) Eeg only measures neocortex with bad spatial resolution Subcortical structures are measured with depth electrodes: used in epileptic patients to localize the locus of seizures Single cell recordings/animal research: specific Polysomnography: measure electrical activity of brain and muscles, gold standard EOG: vertical and horizontal eye movements (REM) EMG: muscle tonus, chin, arms, legs Bruxism: teeth grinding, intense muscle activity that involves entire face Periodic leg movement, restless legs EKG/ECG: HR, to see cardiac anomalies (some heart problems are better diagnosed at night) EEG: human brain is dynamic, multiple frequencies, used to determine sleep onset and different sleep stages, anomalies. Summed up activity of neurons but LIMITED, only captures near skull activity BUT we can make inferences… Freq. and synchronies of neuronal discharge to determine WAVES; Freq; # of cycles/second Amplitude; deviation of signal from baseline (synchronous vs asynchronous-> diff brain areas are doing diff things) Higher wave, higher amplitude, discharging at the same time = neuronal synchrony THERE IS NEVER JUST 1 FREQ/1 STATE: combination of freq at different proportions. Spectral analysis but there is often a DOMINANT freq. 13-30: Beta: desynchronized, fast, awake 8-13: Alpha: resting with eyes closed, slower, more synchronized 4-8: theta: more synchronized, more sleepy/sleep onset, NREM 1-2: THETA WITH EYE MOVEMENT-> REM SLEEP 0.5-4: delta: slow wave sleep, huge amplitude, NREM 3 Rem sleep: ¼ of sleep Non rem sleep: Awake: 5%-> fragmented sleep Stage 1: 5% (transitional between wake-sleep) Stage 2: half of night Stage 3: deep sleep, 15% Hypnogram: sleep architecture: graphs Stage 4 is now part of stage 3 90 mins to complete cycle but start of night more deep sleep, later more rem sleep (for survival, brain needs to get more deep sleep so does it first to get over with it) Naps with previous night sleep: REM Nap with sleep deprivation: deep sleep Nap with partial sleep: REM to complete cycle Sleep is dynamic, we compensate Waking EEG: Central and occipital derivations: C3, C4, O1 and O2 Saccades: saccadic eye movement Waking eeg: eyes closed: slow rolling eye movements, brain is ready to sleep Sleep onset: gradual process, easy to wake up from this stage/not really considered a stage because so fragile, slowing down of firing rate/slowing of brain activity (CORTICO-THALAMIC), eye movements/rolling, diminished responsiveness to outside stimuli and hypnagogic imagery, sleepiness is felt before sleep onset, NREM1, LECTURE 3: Neurosscillations Hz; unit to measure #of cycles per second Alpha; lower activity in occipital cortex Hz; frequency, how fast Amplitude; synchrony which is a neuro correlate of many things EEG flattening; theta gets desynchronized and then synchronized Hypnagogic images appear in theta NREM2: everyone agrees that this is a sleep stage, more stable, less susceptible to interruption/awakening K complex: Looks like cursive k, peak upwards and downwards/2 peaks so bipolar, slow wave, last at least 0.5 secs, perceptual/neurological and neuroplastic roles (thalamocortical gating-> selective perception, if the stimulus is worth attending to (dropping smt but person doesnt wake up but k complex appears) sleep preservation and selectivity Sleep spindle: Burst of sigma/fast activity, neuroprotective processes (less of these in some brain disorders, eg dementia) K complex and spindles represent change from stage 1-stage 2 sleep NREM 3: Delta activity, slow & synchronized waves, most important for survival functions, parasomnias occur in this stage (brain is sort of in 2 states at once, counterintuitive), least responsive to environment (deep sleep in kids is like anesthesia high threshold for perception/perceptual disengagament, low for pain/arousal etc). We get less of this deep sleep with age REM: Brain looks like its awake (paradoxical), arousal/physiological activity (mostly theta and some alpha) Saccadic; eyes are always moving to perceive (scanning hypothesis, are we perceiving the dream world?) Muscle atonia; paralysis so you dont act out your dreams (kids dont have this because they can walk away yet) Waves are desynchronized, face relaxed-> extreme relaxedness, multisensory integration, quasi perceptual state/dreams as perception, area V1 is activated Tonic (rem sleep without eye movements for a bit) vs phasic (eye movements happen again) 1st half; more slow wave sleep, second half more rem sleep If u wake up from deep sleep, u go through all stages again but faster (homeostatic pressures, ideal circadian moments) Sleep microarchitecture: Cap; cyclical, sleep is not monolithic Sleep spindles; represent corticothalamic activity/dialogue with thalamus, theta like pattern/burst/pronounced, time bound, NREM 1-> start of NREM 2 Potential functions; memory consolidation, neuroplasticity, intelligence?? Clinical significance; altered spindle activity in some disorders, global deficits in thalamocortical functioning/loops, change with age New research; generating spindles…will it have a + impact? Maybe the role of spindles changes with age, non-ageist view Spindle density increases following a moto task (eg finger sequence tapping task), new stuff to reorganize, demand characteristics/motivational orientation. Now we have a more modern view on spindles K complex: Nrem, start of n2, spontaneous vs evokes, thalamocortical gating (do i wake up or not), arousal brain perceives) and stability of sleep (u still dont wake up), same genesis as sws Evoke potential; brain perceives smt from environment Sw: slow, synchronous, in neocortex/locally (dolphins and 1 hemisphere sleep at a time), functions; memory consolidation, synaptic homeostasis/brain saturates with synapses throughout the day and at night u are oversaturated so u need to downscale/prune those connections/rebalancing/strengthening/opening new spaces for the morning, restorative functions/biologically most important, reactivity to environment) LTP: learning, instant homeostasis-> more slow wave activity due to sleep disturbances, long-term homeostasis-> plastic changes/cognitive gain LECTURE 4: Recap; significance of slow waves being locally generated-> neocortex and then propagates to entire cortex, hybridity and neuroplasticity Corticothalamic gating-> thalamus receives some info (selective gating) but info/stimulus has to be SIGNIFICANT/RELEVANT ENOUGH TO WAKE YOU UP (works with neocortex in a top-down fashion) Sleep is a GLOBAL brain state (brain stem+ neocortex) Brain waves change drastically from wake-> eyes closed (alpha) arousal state if u start from delta, sleep state if you compare it to wake state Rem: desynchronized, mostly theta, intrusions of other waves too, paradoxical-> u seem to be awake, u look at muscle atonia (to prevent us from acting out our dreams) to confirm that person is actually asleep Scanning hypothesis; u look at the dream world to orient yourself, saccadic eye movements Possible index of dream intensity (low correlation), perceptual engagement Less rem sleep/eye movements for depressed patients Limited evidence that rem is important for learning CAP: sleep is dynamic/stable and you can find regularities/cycles, predictable intervals, it’s anything (not just delta), used as a marker of sleep instability Significance; used in comatose patients to determine recovery/gain of consciousness Cap changes with age, represents arousal in NREM Paradoxical insomnia: sleep architecture is normal BUT reports say otherwise, hypnogram looks fine, so important to look at cap (intrusion arousal markers-> misperceptions but they are subjectively right) philosophy and science/psyc Sleep is homeostatically dynamic, resilient (external demands vs internal needs) Sleep architecture (when and how long) Ultradian; less than 24 hrs Finer microstructures of sleep: Sawtooth = theta (rem) Slide 16/41 (hours awake): VERY IMPORTANT Sleep is regulated by circadian and homeostatic mechanisms, these 2 are INDEPENDENT OF EACH OTHER If ur at peak circadian waking hours, u will be illusionary less tired Homeostatic pressures build up the longer ur awake Sleep deprivation experiment; awake for 36 hrs, delta sleep and time NREM, STAGE 2 AND REM High homeostatic pressure, they sleep Then awake, homeo and circ both work together towards arousal, u start earning homeostatic debt but circadian says this is when u should be awake You pay off your homeostatic debt when u sleep/nap so not ideal for insomniacs (u get a lot of slow wave sleep which is needed for survival) Ultradian in graph means rem, less than 24 hrs. U have rem rebound if u need rem (wake up early every day so during nap u get rem) BUT slow wave sleep is more important Neural control of sleep: arousal system vs sleep-promoting system Sleep is not a state, its a process (those processes are present during wakefulness but you override it) Arousal systems of brain; many networks-> global process, compensation if damage to one system (REM-> some arousal systems are on/cortical arousal but some are off/muscle atonia) Ascending arousal system: (bottom up) Generation of arousal occurs in brain stem Wake control networks: GABA promotes sleep, NE, ACh, DA, HA, 5-HT promote wakefulness Eeg and motor arousal: orexin/hypocretin-> important for rem, projects to brainstem and diencephalon/forebrain, lack of orexin leads to narcolepsy with cataplexy Wake-on, rem-off arousal: cessation in rem 5-HT: complex role NE: projects from locus coeruleus, high discharge in wake, low in NREM, cessation in rem HA: high discharge in wake, low in NREM, cessation in REM. antihistamine-> sedative effect Orexin: arousal promoting, on in awake, off in NREM and REM Wake-on, rem-on: high rem ACh: RF and BF, DA: dreams are like rewards according to freud, hedonic. Parkinsons’ and more daytime sleepiness Glutamate: excitatory LECTURE 5: Sleep promoting systems: VLPO: very important, where sleep is controlled (decision to sleep or be awake), in hypothalamus, mpn, more active in NREM and REM than awake, responsive to sleep deprivation and homeostatic pressure (sleep debt) Circadian system: endogenous signals for alertness VLPO uses GABA: most important inhibitory receptor, everywhere in the brain, associated with sleep promoting circuits, inhibits wake promoting arousal systems Sleep promoting neuron discharges more during sleep, never fully off though: in mpn Rte of spikes; fq, eeg measures multiple neurons, cortical Flip-flop sleep switch system: in the vlpo, determines which of the competing system ends up winning Wakefulness: red; inhibitory, green;excitatory, actively working inhibitory nuclei, orexin/hypocretin/wake promoting/excitatory also acts on nuclei so then the nuclei work in an excitatory way. This is all over the brain. INHIBIT VLPO AND PROJECT AROUSAL PROMOTING NUCLEI Sleep: EXCITATION OF VLPO, IT wins, inhibit arousal promoting stuff, floods brain with GABA Thalamo-cortical regulation of eeg rhythms: - Sleep is defined by eeg patterns (NREM, REM) - Interaction between neocortex and subcortical structures - tonic/desynchronized, rhythmic/synchronized (high amplitude means synchronized-> same rate and same time) Thalamocortical loops: thalamus projects to cortex and cortex reports back to thalamus What controls sleep? - Preoptic area in hypothalamus - Also… - Circadian system - Homeostatic system - Hormonal system - Limbic system - neocortex In a sense, the only true correlate is behavioral: we sleep because we get sleepy. - Different scales. Vlpo: seconds, Switch: seconds, circadian regulation in days, menstrual, seasonal, etc Adenosine: inhibitory neuromodulator of CNS/inhibits wake promoting nts: serotonin, ACh, norepinephrine, blocked by caffeine Accumulates in basal forebrain with sleep debt, diminishes during sleep Coffee naps: u drink espresso, take a nap and then u have more energy arousal promoting nts: Dorsal: where, rhc Ventral: what, rtc Aminergic: serotonin, dopamine, norepinephrine Cholinergic: ACh Activation synthesis hypothesis; dreaming, saw NREM-REM cholinergic activity as a correlate of dreams but this is FALSE. Mapping cat/rat neuroscience to humans is a big nono U can dream in any stage of sleep but the quality differs, arousal/rem is when ur MORE LIKELY to dream. There are no actual neuro-correlates of dreams. Brain activity in sleep: Looking for functional connectivity and anatomical correlates of eeg events in sleeps (eeg stages) SWS: propagated through frontal areas, locally generated, we know this bcs of mri Glucose energy: how much energy neurons are consuming/how active they are, a lot of glucose metabolism when awake (it’s costly for brain to be awake), SWS very little glucose metabolism, rem u consume a little more Nrem: glucose metabolism and cerebral blood flow decreases, overall decrease of activity Rem: more activation, certain areas more active than nrem (emotions and memory), some areas less active than wakefulness (executive attentional areas) Lucid dreaming; pfc becomes more active Pgo waves; initiate rem, neocortex is activated in a bottom-up way, motor and sensory input are blocked and eye movements are generated Rem-off and rem-on cells (brainstem and hypothalamus): specific rem sleep regulating cells, there’s smt fundamental abt cycling between rem and slow wave sleep Brain connectivity: networks, different brain areas are talking to each other, eeg connectivity analysis, ur hugely inter-connencted when ur awake, less connectivity in sleep, slow wave sleep (less connected but more synchronized), rem: ur not getting connections with pfc States to processes: finer granularity and overlap, nrem often used to refer to sws/deep sleep, you can have sleeplike/dream-like processes during wake and vice-versa, (WAKEFULNESS IS NOT MONOLITHIC, DIFFERENT TYPES OF “WAKE”), processes are discrete but the states overlap What is sleep quality? normal/eeg measures and subjective feelings (difference between objective and subjective measures), SWS is the most important for sleep quality AND continuity (more consistent sleep all the time/ good sleep schedule) may be more important than duration. Paradox; u CAN feel better when u dont sleep enough but this is short-lasting LECTURE 6: Circadian rhythms MANY rhythms with different time scales There is an endogenous (circadian/process c and homeostatic/process s) and exogenous (environment) part to our cycle Sleep regulation: Homeostatic: debt, pressure, Circadian: independent of other systems, approximately 24 hours (realistically a little over 24 hours), adaptability to world and responsiveness to our internal needs Ultradian: less than 24 hrs, basically SLEEP ARCHITECTURE, dependent on homeostatic and circadian pressures Circadian system; brain: SCN: circadian master clock, oscillator, persistent and predictable endogenous rhythms Other organs: every tissue has its own circadian rhythm, all controlled by SCN Zeitgeber: external things, own endogenous rhythm, strongest to weakest-> (light, food, active-rest, social cues) etc, participate in circadian entrainment: how u adapt to world around you, their effect depends on circadian phase of the organism Is SCN is lesioned, everything is messed up, desynchronization Transplanting scn into hypothalamus restores rhythm Melatonin: created by pineal gland, most important endogenous hormone for sleep, acts on SCN, stimulated by darkness, suppressed by light, opposing action with cortisol, regulates breeding patterns, involved in immune function 3 am: melatonin and cortisol overlap: preparing to wake up but you’re still sleeping, arousal promoting hormone, this is why u have nightmares in the morning Melatonin can be studied peripherally, u can capture NTs directly bcs of blood brain barrier, we make assumptions, melatonin crosses BBB so u can measure it in blood Body temp drops, bp drops, growth hormones are expressed sharply, immune markers Melatonin and scn work tgt thru eye ball movement: Melatonin and seasonal changes: more melatonin in winter Circadian system: ganglion cells in retina: communicate with scn thru retino-hypothalamic tract, dont have much to do with vision but WORK WITH melatonin, intrinsically photosensitive/react to light, melanopsin/light sensitive protein, control pupil dilation, also project to vlpo, melanopsin sensitivity to blue light (daylight is a mix of all colors) so u want NO blue light at night Non-image forming visual system: higher threshold of excitability Retoni-hypothalamic tract Direct connections from retinal ganglion cells SCN IPRGC: slow&progressive response Need higher intensity light (than cones) After light off keep firing for some time There is a hierarchical organization: principal oscillator/scn to genes You can artificially create a shift in circadian rhythms: circadian phase synchronized by light exposure; turn on light a little earlier every day and after a few days, new rhythm (like traveling across time zones) Circadian rhythms in sleep; constant routine is a protocole where u bring smn in a lab and keep them in constant conditions, no social cues/clocks, eliminate zeitgeber, disrupt sleep patterns and reveal endogenous patterns, average circadian cycle is 24.15 hrs Endogenous aspects of circadian regulation: free running rhythms in constant conditions (eg blind individual/doesnt have access to important zeitgeber, LIGHT)-> desynchronized, other zeitgebers have a weak circadian entrainment Constant environment& c patterns: siffre went to a cave, 24hr (robust and persistent) to 18-52 h! (responsive) Chronotype: morning/night person, subjective measure, varies with gender&age What influences chronotype? Planet were on, many factors (genetic, individual, environmental, social, etc) LECTURE 7: Chronotype correlates: early vs late (misalignment or smt more intrinsic?) Individuals that live in northern countries tend to be of the morning chronotype (the sun or social factors?) Temporary or permanent neural changes if your sleep is impaired, also more likely to remember negative if you’re sleep deprived -> all contribute to circadian misalignment Chronotype issues: - Mixed chronotypes - Extreme phase delay: misalignment with social expectations and demands - Covid 19: many realigned with their “natural chronotype” - Polyphasic sleep: no such thing as “purely biological sleep”, sleep in chunks -> evidence in medieval manuscripts (described as first and second sleep), “seen as natural sleep but no consensus”, WEIRD: western educated industrialized rich democratic. Consensus panel says it’s not good but it really depends from person to person Circadian disorders: often produce insomnia BUT not the same as insomnia (i cant sleep now vs i cant sleep) Entrained: planetary rhythms and social life are aligned Phase delay: night owl, night chronotype Advanced: morning person Fragmented: sort of polyphasic, new parents/caregivers, typically undesirable but depends on context, in kenya/communal area women with young children felt better getting this kind of sleep bcs ATTITUDES MATTER Free running: no resetting, often in blind individuals who cant be entrained by the light, Most significant circadian disorder: irregular sleep wake rhythm disorder ​STUDY: The body's ability to awaken from a coma after severe brain injury is tied to its maintenance of its natural circadian rhythms Consequences of circadian disorders: - Can lead to insomnia - attention/mood difficulties - Social isolation (phase advance (morning chronotype)/everything happens in the evening and non-24 hour rhythms) - Long term: GI issues, cardio, mood, cancer issues Mood regulation: SCN (daytime/nighttime), HPA axis (stress) SAD: depressed in winter better by summer, high rates of suicide Bipolar: manic episodes occur in summer, mild sleep depression - Environmental factors (photoperiod; natural light), social/cultural, biological Treatment of circadian disorders: - Circadian entrainment - photo/light therapy: arousing/wake effect with lamp, so scn can stop making melatonin - Melatonin, does it actually work or is it placebo? Uclear bcs we can only measure its effects peripherally Jet lag: temporary circadian misalignment-> requires entrainment to host environment Work better when u go “back in time”: harder to sleep early than it is to sleep late/accumulating homeostatic pressure (europe to canada is easier), takes about 3 days to reset (entrain yourself to be a morning person in your time zone) Social jetlag and teens: adjusting to social pressures, tend to be late chronotype (delaying school start time improves grades and performance, less behavioral issues) Catching up on sleep during the weekend is not a great idea bcs u reduce ur homeostatic pressures and have trouble waking up early during the week again Shift work: - Produces circadian misalignment - Insufficient sleep - Shift workers often compensate on days off - Opposite to insomnia/delayed sleep: they get exposed to sunlight at inappropriate times - Solution: avoid blue light exposure, wear blue light blocking glasses - Social jet lag and shift work: metabolic/cravings/obesity, diabetes, impaired cognition, sleep disorders Younger ppl are more likely to experience social jet lag, tolerable for 25 mins ish Solutions: flexible work schedule, later school start, eliminate daylight savings time Fluorescent street lamps: good for ecology but having them late at night can contribute to chronic circadian issues Sleep justice: light pollution, floodlights for safety BUT sleep is significantly impaired when it already is probably already bad sleep (circadianly challenged) + sleep equity LECTURE 8: Bright light exposure in ICU: not enough daylight (ICU delirium-> when ppl come out of anesthesia, they can have a moment of temporary disorientation) so they add bright lights at the RIGHT TIME, neonates-> entrain circadian rhythmicity in preterm babies which improves weight gain and shorter hospital stay Circadian rhythm: all tissues have their own oscillators Intrinsically photosensitive retinal ganglion cells (ipRGC), melanopsin (light sensitive protein), melatonin (darkness sensitive hormone more produced in dark), RHT, period, phase Phase shifts = circadian disorders Functions of sleep 1: adaptive inactivity - Sleep is ubiquitous in the animal kingdom/biological imperative but varies, total sleep deprivation = death - 6 theories of sleep function 1. Host defense, immune system (sleep and immune, correlational link) Organisms sleep more with disease, possibly to conserve energy to fight a disease, but not clear why you need to be unconscious during sleep. Bed rest-> increase in nrem and decrease in rem when sick (SWS is where you heal) but you have more FRAGMENTED sleep, more sleep = more immune system cells 2. Conservation of energy (SWS especially), energetically taxing to be awake Econ. metaphor Trade-off: temporary inability to interact with environment (biological investment) but metabolic benefit for whole body (costly, thermoregulatory efforts, waking effort), less glucose use in NREM SWS, energy allocation model. Caloric conservation (lower body temp, hibernate, reduced energy use), short sleep is associated with risk of diabetes/metabolic system, obesity, craving for carbs 3. Restoration of energy stores (energy capacity, potential for learning) 4. Glymphatic function: removing toxic byproducts, extracellular stuff (glial cells acting like the lymphatic system CNS), more active in sleep, eliminates neurotoxins, including beta amyloid (alzeimers), astrocytes, they also bring in nutrients 5. Restoration of performance (cog. functions), need to prune whatever saturated connections you made during the day  6. Sleep serves connectivity/plasticity Brain connections change over time, pruning occurs during sleep, fire together wire together (LTP, synaptic connections) Tononi’s synaptic homeostasis hypothesis: 1. New learning happens by synaptic potentiation (suspicious coincidences) 2. synaptic potentiation should mostly occur during wake (reality vs dream) 3. Renormalization of synaptic strength should mostly happen during sleep bcs there can be moments when ur brain is oversaturated (u just cant learn anything new), NREM sleep, hippocampus/memory and neocortex communicate Neurogenesis: only in hippocampus do new neurons grow in adulthood Most likely many functions Evolutionary function of sleep: Sleep appears in any organism with a neuronal-glial network (even animals that live in deep sea/no light have some form of rhythmicity) -> need quiescence period for neural architecture There is an inverse relationship in herbivores and hours of sleep needed (elephants need to eat more so they sleep less) No such relationship in carnivores Same sleep stages can play different roles in different animals, brain is different/changing Unihemispheric sleep: dolphins, they might need to come up for air, prevent drowning, migratory birds have to sleep in air (these animals only have unihemispheric sleep when they need to, so if migratory bird is on ground it might not have unihemispheric sleep) LECTURE 9: NOT INCLUDED IN MIDTERM 1 Functions of sleep, part 2: INCLUDED IN THE MIDTERM? Some new theories: planetary adaptation, 24h rhythm, no more strong visual input, internally generated activity, rem is important for flexible neural connections/plasticity, occipital functions are not being taken over by any other senses during day so at night it gives a chance to prune the saturated visual input? Developmental shifts in function: Does everything get worse when we age or is it a transformation as we age? Reorganization to repair (role of REM differs depending on age) (chronic) Sleep deprivation: Many negative effects: chronic diseases, impaired cognitive functions/performance, mood disorders (sleep deprivation is an amplifier is you are predisposed to these disorders/diseases)-> causes: lifestyle (circadian misalignment), shift work, sleep disorders You can have temporary symptoms from one bad night of sleep but chronic sleep deprivation is more concerning Fix sleep-> depression symptoms go down (we dont know much about the causality) Acute sleep deprivation: Randy (stayed awake for 11 days 25 mins), stanford-> william dement Effects: slow reaction time, early mornings were hardest (more pressure for sws), waking dreams/hallucinations, most likely had microsleeps, quasi-psychotic symptoms/paranoia, disoriented in time, body sensations (pain and burning in eyes, etc) He then slept for 14 hours and 40 mins (a lot of sws/more pressures for sws, not a lot of rem, later parts of night he has a lot of rem) Memory and sleep: Incubate an answer, sleep on it… Sleep functions: restoration of performance/cognition - Memory, reflexes, attention, mood, emotions, etc Sleep helps you remember and to forget (memory consolidation-> stabilize memories, extract what’s important/pruning, create associations between what you’ve learned, dissociate emotions to form semantic memories) you always remember more after sleeping/napping Memory; temporal scale sensory->stm->ltm declarative/explicit: facts, experiences (autobiographical is time travel, allows us to imagine the future): semantic and autobiographical are BOTH accessible to consciousness nondeclarative/implicit: know how (procedural, conditioning, priming)-> not generally accessible to consciousness 2 important subcortical structures: Hippocampus (binds memory ingrams/cortical traces together, DOES NOT STORE MEMORIES) and amygdala (emotions) Memory consolidation: active memory and recalling a memory can pollute it, ever-changing memories Long-term storage; neurophysiology: LTP, fire together wire together/hebbian learning, strengthening of synapses/creating stable memories Memory consolidation: In animals: evidence for neural replay during sleep, in humans it takes place via hippocampus -> papez circuit; it’s an active process; transfer/triage of newly encoded memories, a temporal process/takes many days, has daytime and nighttime components How to study role of sleep in memory consolidation: - Observational; correlation - Sleep deprivation/selective sleep stage deprivation - Targeted memory reactivation; maybe we can stimulate replay of memories during sleep; classical conditioning Sleep inertia: proper waking up after waking up Group D had better performances because they slept Sleep before learning: if youre sleep deprived, you still remember negative stuff the same way participants who got sleep would Main models of sleep-dependent memory: - Sleep protects memory from forgetting - Rem and nrem is for memory consolidation - Sleep facilitates forgetting - Dual process (nrem and rem do different complementary things), sequential (do follow one another; sequence/sleep architecture follow each other) - Active systems consolidation (brain elements are coordinated) Rem sleep and memory consolidation: Rem and dreaming-> what abt memory Rem increase in animals after learning Rem deprivation-> impaired learning in animals Dual process models: - nrem and rem do different complementary things - Sws strengthens declarative, rem improves procedural - Sequential hypothesis: sws and rem not as important as THE CYCLICAL SUCCESSION OF THESE 2; sws strengthens connections between new engrams and rem integrates newly learned memories into larger autobiographical networks/state of associativity. Balance: stability vs flexibility of the cognitive system (u need updates but not too many updates) Active system consolidation: - Eeg, hippocampal-neocortical dialogue through-> slow waves, spindles, hippocampal sharp waves/ripples LECTURE 10: