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20 Cards in this Set
- Front
- Back
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retinohyothalamic pathway
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branch of optic nerve - from retina to SCN. special ganglion cells have melanopsin photopigment, responds via special pathway, resets bio clock according to light stimuli
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what is function of period and timeless gene
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Per and Tim protein, levels increase throughout day as the increase, trigger slepiness, whih triggers neg fdbk loop to stop pro prdn
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what do long slow waves on EEG indicate?
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low level activity (prob stage 3 or 4) there is synchrony of response among neurons
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retinal ganglion cells, secrete, pathway, function
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special cells that respond to light w melanopsin (sp kind of photpigment) send info to SCN,
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biochem factors of circadian rhythm Tim/Per, SCN
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Tim and Per proteins increase during day, ultimately trigger.
SCN informs (at lower light) Pineal gland to release melatonin, which causes drowsiness. |
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stage 1-4 sleep
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1) alpha waver -8-12 per sec, jagged low voltage
2) sleep spindle / K complex 3) |
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sleep spindle
k complex slow wave sleep |
k are higher amp than sleep spindle, both characteristic of stage 2
SWS waves characteristic i stage 3 & 4 |
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recticular formation- anatomy
pontomesencephalon |
1)part of midbrain - extends from medulla to forebrain, regulates arousal
2)part of recticular formation, release glutamate & ACh,has to do with wakefulness (cortical arousal) |
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what released: Excite or Inhib
pontomesencephalon loecus coerelus Basal Forebrain Hypothalamus Dorsal Raphe & Pons |
ponto - ACh & Glutamate - Ex
loecus - norepi - Ex - info storage basal Fbrain (2) ACh: Ex thal &cortex, GABA: Inhib thal & cortex hypothal-Histamine & orexin - Excite Pons/Dorsal Raphe - Seratonin, Excite (interputs REM sleep) |
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PGO waves
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(ponsGeniculateOccipital) originate in PONS, accumulate if REM deprived, hallucination behavior
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insomnia, sleep apnea, narcolepsy, cataplexy, and periodic limb movement syndrome.
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impaired ability to breathe while sleeping.
Narcolepsy – sudden attacks of sleepiness during the day (issue w orexin deficiency?) Cataplexy – attack of muscle weakness while you are awake, triggered by strong emotions: anger , excitement) Periodic limb movement syndrome – repeated involuntary movement of the legs, involuntary kick before you are about to fall asleep. |
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activation-synthesis and clinico-anatomical hypotheses
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Dreams are the brains attempt to make sense of info that might have been haphazardly input by the pons, input from pons can activate amygdala, which is involved w strong emotional processing, therefore dreams may have strong emotional aspect
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endogenous cicannual & circadian
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innate /internal rhythm (even w/out zeitgeber), circanual is seasonal (migration) circadian is approx 24 hr
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caffeine
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increases arousal b/c blocks adenosine receptors - adenosine accumulates during wakefulness and eventually triggers sleepiness
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sleep stage 1
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alpha wave present when you are elaxed
stage 1) sleep just begun, EEG irregular, jagged low voltage wave, brain activity slows |
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sleep stage 2
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sleep spindles - 12-14Hz waves during miin 1/2 second bursts
K complex sharp High amplitude NEG wave follwed by smaller slower positive waves |
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sleep stage 2
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sleep spindles - 12-14Hz waves during miin 1/2 second bursts
K complex sharp High amplitude NEG wave follwed by smaller slower positive waves |
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sleep stage 3 & 4
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SWS slow wave sleep: EEG shows slow large amplitude waves, slow HR & Breathing & brain activity
highly synchronized neural activity |
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REM (all previous were Nrem)
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rapid eye mvmnt
AKA paradoxical sleep b/c motor /skeletal muscles very relxed, but brain very active happens later in the eve, this is the stage whre dreams happen, REM section increases w each cycle |
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order of sleep cycle
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1 2 3 4 3 2 REM 2 3 4 3 2 REM
* 3&4 predominate earlier in night, REMpredomiant in the later part |
