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Week 6

by: Emma Notetaker

Week 6 NSCI 4510

Emma Notetaker
GPA 3.975

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week 6 lecture (only one class)
Biological Psychology
Dr. Colombo
Class Notes
25 ?




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This 4 page Class Notes was uploaded by Emma Notetaker on Thursday February 18, 2016. The Class Notes belongs to NSCI 4510 at Tulane University taught by Dr. Colombo in Spring 2016. Since its upload, it has received 21 views. For similar materials see Biological Psychology in Neuroscience at Tulane University.

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Date Created: 02/18/16
Thursday, February 18, 2016 Week 6 Sleep • all animals sleep • ideas about why we sleep: • energy conservation during sleep humans not equipped to function during the night (disadvantaged; no night vision, won’t • accomplish survival tasks) - SO we sleep • body restoration - we need to restore our energy supplies • memory consolidation: short term memory into long term memory • sleep research • started 1930’s other research methods include: • • studying ocular movements during sleep • muscle contractions during sleep • EEG • electrodes on scalp • measures cortical firing/activity firing must be synchronous to create wave pattern • • waves described in amplitude and frequency • stages: • waking • low amplitude waves • not synchronous - looks noisy mixture of high frequencies • • stage 1 slow wave sleep: • alpha rhythms - 9-12 Hz (cycles/second) —> also seen in very relaxed awake person (meditating, etc) • vertex spikes accompany actual sleeping • non-responsive to whisper, BUT may think that they are not asleep earliest stage - in between sleep and waking states • • stage 2 SWS • K complexes: large negative wave (big amplitude) • sleep spindles: burst of activity • first evidence that person is ACTUALLY asleep • stage 3 SWS delta waves appear: very slow (1Hz) • • high amplitude, low frequency • stage 4 SWS • delta waves appear at least 50% of the time • REM • rapid eye movement takes about 60 minutes to get to REM sleep • • not synchronized, higher frequency with low amplitude • muscle/postural tension disappears • paradoxical sleep: brain is very active but muscle tension is lost • breathing and pulse irregular and fast 1 Thursday, February 18, 2016 • go from stage 4 BACK to stage 2 before REM - don’t go directly from delta to REM • Process: • down through stages, back to 2 then REM • short bout of REM • back down through stages, followed by a longer period of REM • as you go on, REM increases in length while SWS decreases in length each time wake NREM REM muscle tone higher less none EEG low amplitude, noisy large amplitude with lowsimilar to waking - low frequency amplitude and noisy sensation and vivid, externally dull or absent vivid, internally perception generated (thoughts generated (NOT driven by external sensory) world) thoughts logical progressive logical perseverative illogical, strange movement continuous and episodic, involuntary commanded but voluntary inhibited (probably evolutionary - so we don’t do crazy things in our sleep) Propeeryy SWS REM Heart rate slow decline variable with high bursts breathing slow decline variable with high bursts thermoregulation maintained impaired brain temperature decreased increased cerebral blood flow reduced high postural tension progressively reduced eliminated knee jerk normal suppressed phasic twitches reduced increased eye movements infrequent, slow, uncoordinated rapid, coordinated cognitive state vague thoughts vivid dreams, well organized growth hormone secretion high low cerebral cortex activity (neural many cells reduced and more increased firing rates, tonic firing rates) phasic (sustained/increased firing) 2 Thursday, February 18, 2016 Property SWS REM sensory-evoked potentials large (often respond to sensory reduced (tend to ignore sensory input) input) • during REM, there is not a lot of rest going on - increased heart rate, blood flow, etc. doesn’t support the energy conservation model of sleep • • overall, most properties of SWS are opposed by REM (see table above) • during REM, brain ignores external world • in SWS, brain does attend to SWS but is resting • physiological changes that occur during dreaming (REM) • sensory input is blocked due to presynaptic inhibition (stopping neurotransmitter release) • external perception diminished • lose attention due to aminergic (monoamines - serotonin, dopamine, norepinephrine) decrease in activity • brain stops suppressing all the extra noise, so you can’t attend to everything • cholinergic hyper stimulation - overstimulating amygdala and limbic system which causes intense emotion • rat has small area of cortex relative to brain - flat, not a lot of processing power • dolphins have huge cortex (relative to brain size) - LOTS of folds, very high surface area • half of their brain sleeps at once - stage 3 sleep restricted to one hemisphere while the other one is alert/awake • over human life span: • during first 2 years of life - sleep a LOT more and REM especially increased (infants spend 2/3 of day sleeping, 8 hours of that is REM) • REM very important in early brain development • as you age (after the first few years) - sleep slowly decreases but REM hours stay fairly constant mechanisms of sleep • • anesthetics (barbiturates, propofol, ketamine, NO, isoflurane): • GABA agonists (inhibitory) • glycine agonists (also inhibitory) • most are antagonists for glutamate: excitatory • most antagonize cholinergic (ACh): excitatory • stimulate GABA/glycine —> sleep • stimulate glutamate/ACh —> waking • brain systems view: • Bremer’s theory: isolated brain • reduced input to forebrain —> sleep to test hypothesis: isolated cephalon • • transect below medulla, get brain that still goes through sleep stages • isolated brain still generates EEG sleep waves associated with different stages • REFUTE this theory: got rid of the sensory input but the brain still went through stages • whatever causes the brain to sleep is above the peripheral level • isolated forebrain: • transect area between midbrain and pons • brain is constantly in SWS ONLY (no waking or REM stages) • —> forebrain responsible to SWS 3 Thursday, February 18, 2016 • current view: • SWS generated in basal forebrain reticular formation (runs through brainstem) activates brain from sleeping state into • wakefulness • nuclei in pons associated with REM generation • noradrenergic input from locus coeruleus • hypothalamus integrates all the states - controls all of them • orchestrates when you’re awake vs. asleep via hypocretin • • hypocretin made by neurons in lateral hypothalamus • stained by immunocytochemistry • normal person secretes hypocretin • narcoleptic person has very little hypocretin - deficient (hypocretin can’t do its job properly) • excessive drowsiness sleep regulated by cellular level as well • • record neuronal activity • in awake animal, most neurons in motor and parietal cortex “on” and some “off” • in sleeping animal, most neurons “off” but a few are “on” • in animal forced to stay awake, neurons start to become less responsive • more are “off” than in regular awake state experiment: rodents learn to pick up sugar pellet • • just before a miss (about 1/2 a second), a lot fewer neurons are fired • can predict hit or miss by monitoring individual neurons in the brain • % of “off” neurons is related to success rate • more noticeable in the motor cortex than parietal (more predictive in motor) 4


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