Carlson

Sleep (p.289 – 314) Stages of Sleep Muscle – EMG Eye – EOG During wakeful you have alpha and beta o Alpha = 8-12Hz (reg medium freq) when relaxed o Beta = 13-30Hz (irreg, low amp) shows desynchrony Stage 1: o Theta = 3.5-7.5Hz -> firing in neo becoming more synch (eyes move a bit) Stage 2: o 10 min later o Irreg o Sleep spindles (sudden sharp wave forms usually only in stage 2) -> 1 per min  Triggered by noise o K complexes (12-14Hz short bursts) -> usually 2-5 times a min in stage 1-4  Memory and correlation with IQ  Neural inhib? Stage 3: o Delta = less than 3.5 -> high amp Stage 3 has 20-50% delat, 4 have 50% 3& 4 are slow wave o Most imp is 1Hz high-amp biphasic…first part of wave is down state (inhib) than up state (excit) After 90mins or 45min after stage 4 we reach a desyn state with spinkle of theta waves…looks like stage 1 -> REM o If awaken during 4 they are groggy if during REM they are not o 20-30 min bout of REM o Thus 8 hr will have 4-5 REM periods o More stage 2 and REM later in sleep

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Mental Activity During Sleep Rate of blood flow during REM high in visual association, low in primary visual and prefrontal Measure eye movement and wake up during REM, eyes would be moving as if it were actually happening. Even same brain mechs active as if it were really happening…i.e. motor mechanisms if dreaming about moving Nightmares in stage 4

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Disorders of Sleep Insomnia 25% occasionally and 9% reg Most insomniacs underest the amount they sleep Want hang over free drugs Sleep apnea: CO in blood stims chemoreceptors and person wakes gasping for air

Narcolepsy Sleep bout for 2-5min (usually monotonous work) Cataplexy = muscle weakness (usually strong emotions) Sleep paralysis = before or after sleep, REM may intrude and the person dreams -> hypnagogic hallucinations 1 in 2000 Gene on 6 o Code for orexin/hypocretin (A and B receptor with mut in B) o Immune system may attack these neurons early in life Treat with stims for sleep attacks, antidepressants for REM sleep phen Modafinil

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REM sleep behavior disorder Associatied with parkinsons Act out dreams A-synucleinopathies (protein in degraded neurons i.e a-synuclein) Benzo tranq

Problems Associated with Slow Wave Nocturnal enuresis = bed wetting, somnambulism (sleep-walking), pavor nocturnus (terrors) Sleep walking (not acting out dreams) These are during stage 4 Sleep related eating disorder Use dopaminergic agonists or topiramate (antiseizure), provoked by benzo agonist (used for insom)

Why do we Sleep? Rest, learning, brain devo

Functions of Slow Wave Only warm blooded vert (mammals and birds) have REM with paralysis, desynch, and rapid eye Some sleep one hem at a time Effects of Sleep Dep o Human Studies  No phys stress resp to sleep dep…so not body rest  Cog effects…so brain rest  7% of stage 1 and 2 made up with dep, 68% of 4, 53% of REM  Highest brain activity during wake, show most delta during sleep and lowest met activity during slow wave  Get rid of free radicals that would cause oxidative stress  Fatal familial insomnia results in damages thalamus = def in attention and memory, dreamlike confusion, autonomic and endocrine system issues, insomnia  Sleep disturbances and you get reduced spindles and K -> no slow wave -> brief REM o Lab Animals  Stop sleep with exercise and they looked sick with no grooming, couldn’t reg body temp, weightloss Effects of Exercise on Slow-wave o No effect Effects of Brain Activity on Slow-wave o Motor activity before sleep, increased slow-wave activity in those areas o Stage 4 increased

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Functions of REM Rebound phenomenon = spend more time in REM REM the most during brain devo…maybe neuro plasticity too!

Sleep and Learning REM wake up and clear headed, slow-wave and groggy 9am test -> 7pm test…one group 90min nap (measure who went through REM) o Those who didn’t nap did worse than directly after training o Those with slow-wave did same o Those with REM did better o Slow wave for dec, and REM for non Learning spatial maze…same brain areas also active during slow-wave, but not in REM o May have thoughts related to task when awoken here

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Physiological Mechanisms of Sleeping and Waking Chemical Control of Sleep Rebound in only the hem deprived in dolphins Adenosine (nucleoside neuromodulator) -> triggered by fall of glycogen Genes for adenosine deaminase vary…G/A and takes more time to degrade so 30min more in slow-wave than G/G

Neural Control of Arousal AcH o Pons and basal forebrain promote activation and cortical desynchrony o High in hippo and neo during waking and REM, low during slow-wave o Elec pons and release AcH, but deactivate neurons in basal forebrain and then stim pons -> no longer seen o Drugs activating them cause wakefulness Nore o Locus coeruleus in dorsal pons (spread to wide areas) o High neuronal firing during wakefulness -> low in slow wave -> zero in REM o Stim of neurons via opto (ChR2) caused waking, inhib (NpHR) inc slow-wave o Activated LC neurons and inc vigilance Sero o Raphe nuclei in medullary and pontine of reticular form o Stim raphe -> locomotion and cortical arousal o PCPA stops sero syn reduces it o Repeated motion = more sero, directed movement = less sero Histamine o Anti-his block H2 in brain and sleepy o Tuberomammillary nucleus (TMN) or hypo…project to cortex, thalamus, hypo, basal gang, basal forebrain o To cortex it stims AcH neurons o High during waking, low in slow wave and REM Orexin o Lateral hypo o Neurons project all over and have excit effect o High will alert, slow in quiet waking, slow-wave, and REM…highest during exploratory behavior o Modafinial release orexin from TMN which activates histaminergic neurons to stim wakefulness

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Neural Control of Slow-Wave Sleep

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Homeostatic o By adeno Allostatic (reactions to stressful events in enviro) will override homeo o Hormonal and neural, or orexin in hunger Circadian Von Economo -> patients slept all day had damage at junction of brain stem and forebrain o Some showed insomnia -> damage to AH (preoptic area)…forms inhibitory connections with brains arousal neurons o Damage area and insomnia…stim and sleep o Ventrolateral preoptic area (vlPOA) some in median preoptic nucleus (MnPN) o **These inhib areas receive inhib inputs from some of the same areas they inhibit (tuberomammillar, raphe, locus) o Mutually inhib so impossible for both regions to be active at same time Flip-flop good because fast transition…bad because circuits can be unstable o Orexin stabilizes in wakeful state o Mice with mutation switched more often Adenosine agonist into vlPOA activated neurons there, decreased histaminergic neurons of tubo and increased slow wave What controls the orexinergic neurons? o Signals from bio rythmes and nutrition o Hunger activates them, satiety inhibits them o Are inhibited by vlPOA neurons

Neural Control of REM Flip-flop AcH neurons in dorsal pons fire at high rate during REM REM-ON cell increases activity some 80sec before REM So maybe AcH is the neuron? NO o Region in dorsal pons, ventral to locus…sublaterodorsal nucleus (CLD) o Ventrolateral periaqueductal gray (vlPAG) has REM-OFF o Mutual inhib o During waking REM-OFF receives input from orex from LH (also nore, and sero) o Once sleep begins orex stops and it swtiches to REM-ON REFER to fig 9.2 Neurons ventral to REM-ON leave it to excite inhib interneurons who synapse on motorneurons o Damage here and they act out dreams o Maybe motor movements are practices here REM-ON also stim neurons in thalamus for cortical arousal

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o Also send to medial potine reticular formation, which sends to AcH neurons in forbrain to cause cortical desynch o The AcH neurons to dorsal pons of tectum for eye movement Pontine AcH connect to neurons in lateral preoptic to cause erec Fig 9.23