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Exam 2 Study Guide

by: Emma Notetaker

Exam 2 Study Guide NSCI 4510

Emma Notetaker
GPA 3.975

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Comprehensive study guide. Includes all lectures and research article information.
Biological Psychology
Dr. Colombo
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This 18 page Bundle was uploaded by Emma Notetaker on Tuesday March 8, 2016. The Bundle belongs to NSCI 4510 at Tulane University taught by Dr. Colombo in Spring 2016. Since its upload, it has received 111 views. For similar materials see Biological Psychology in Neuroscience/Psychology at Tulane University.

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Date Created: 03/08/16
Tuesday, March 8, 2016 Exam 2 Study Guide 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 Tuesday, March 8, 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 Tuesday, March 8, 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 Tuesday, March 8, 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) Biological Rhythms • Herb Zucker: research on rhythms • pens count rotations as animal goes around wheel each black dot is one revolution • • showed that animals tend to show circadian rhythms • rats more active in the dark (more running) • with artificial light/dark - showed rhythm • with NO information about light and dark (isolated room) - still show patterns of activity that are still approximately on circadian rhythms natural rhythm is a little longer: 25 hours • • MUST have internal generator that controls rhythm with longer “internal clock” • external cues: zeitgeber • when period is tuned into zeitbgebers: entrainment • when there are no zeitgebers: free running • area of the brain responsible: hypothalamus specifically suprachiamatic nuclei (sit right above optic chiasm) • • if you lesion this area, animals no longer show rhythmic activity • lesions disrupt all cycles (NOT just sleep/wake) • temperature • alertness • growth hormone (released in SWS) 4 Tuesday, March 8, 2016 • cortisol (drops off throughout the day, spikes at night during sleep) • potassium graph slide 4: proving use of SCN • • circadian activity in constantly lit environment: cycle will be slightly longer than 24 hours • completely dissociated with any external cues • SCN lesion: sleep cycle is not clustered, randomly patterned • temperature also affected • cells intrinsically rhythmic (can take them out and isolate from brain) put them in culture, continue to show rhythmic release of vasopressin • • light hits retina and goes back to LGN of thalamus • info from left and right eyes goes to both thalami • 3 opsins in cones, rhodopsin in rods • retinohypothalmic pathway: goes directly to SCN from retina • each SCN gets information from both eyes ganglion cells associated with SCN has its OWN opsin (different from that of rods and • cones) - specific to this pathway —> melanopsin • rhythmic oscillations generated by the SCN • feedback from zeitgebers entrains us to follow the daily light/dark cycle • sufficiently rhythmic so that with entrainment it matches the daily cycle • molecular clock: SCN (in flies and mice) - KNOW THIS MECHANISM clock and cycle are necessary for free running • • transcription factors (proteins) - driven by external signals • clock protein (circadian locomotor output cycles kaput) • cycle protein • form heterodimer and interact with portion of DNA on 2 different genes • 1. per gene • 2. cry gene • when they interact with promotor region of the gene, cry and per proteins synthesized • cry and per protein subunits bind together and regulate many cell systems • increase or decrease output of the cell • presence of these proteins INHIBIT clock and cycle from binding (negative feedback) • stops synthesis of cry and per • eventually, per and cry degrade, so clock and cycle can again bind • glutamate increase from retinohypothalamic tract (presence of light) entrains this cycle • stimulates production of per and cry (excitatory) • does not stimulate in absence of light • if mutation of both alleles for clock and cycle transcription factors —> NO CLOCK/CYCLE • with normal light and dark cycles, still rhythmic activity (due to glutamate) • with no light, do not show free running cycle but COMPLETE disruption (arhythmic) - no circadian rhythms at al • in the absence of clock, glutamate entrainment is enough • individual differences (night owls, etc.) depend on levels and composition of clock and cycle proteins • circannual rhythms: • change in coat (rats in fall develop silvery coat) • reproductivity levels • can be mimicked in the laboratory • partially regulated by the thalamus • regulated by changes in the length of the day (winter has shorter day length, etc) 5 Tuesday, March 8, 2016 • EEG • measures temporal characteristics of brain activity (firing of neurons over time) measures tiny changes in distribution of ions • • as nerve fires, sodium goes in (EC more negative), then goes back out (EC more positive) • if cells not firing in synchrony, random scatter • if synchronized, EEG is sinusoidal wave (add together) • can be measured at different places\ • alpha rhythms and beta rhythms can be happening at different places of the brain how is rhythm generated? (both hypotheses contribute) • • 1. patterns of excitation and inhibition • somehow, neurons tune up together (clapping in class example) • many neurons interconnected (via association fibers) - synchrony can come about via excitatory and inhibitory processes • share/distribute timing function based on patterns of excitation and inhibition 2. central pacemaker - leads the neurons • • one neuron oscillators (in thalamus) • stimulate thalamus (short pulse) —> get rhythmic bursts which become single spikes • some neurons intrinsically (when stimualted) tend to fire rhythmically —> these are in the thalamus • then thalamus signals to the cortex rhythmically voltage gated channels control this • • 2 neuron oscillators • constant excitation (NOT rhythmic) • excitatory neuron fires on inhibitory neuron • excitatory cell spiking • as we continue to give constant input, inhibitory cell become excited and eventually shuts excitatory cell down (once inhibition outweighs excitation) —> OFF period • once excitatory one shut down, then inhibitory stops being excited, so excitatory works again • continues…leads to rhythmicity resulting from constant excitation Research Articles • Lineus (background info): • awake: activated brain processing data from outside world and makes decisions about behaviors (directing actions) asleep (SWS, nREM): processing system offline, doesn’t process data from outside world • • asleep (REM): internal representations of outside world become input (NO outside processing) • actions are summoned by not executed - paralyzed • these actions become PART of the input (because they can’t be carried out) • due to the fact that this movement can’t be executed, they become bizarre inputs “The Psychotomimetic Nature of Dreams: An Experimental Study” • psychotomimetic states inventory (PSI): measures psychotic-like experience • hypothesis/research question: similarities between dreaming and psychosis? • people who have psychotic episodes are no different than people who are dreaming • awake schizophrenia is equivalent to normal people dreaming • people awakened from dream state will 6 Tuesday, March 8, 2016 • methods: correlational study - looking at relationships between states and reports of psychotic thinking compared relationships between different states and self-reported PSI states • • states: • NW: dream - natural waking (unlikely to be awakened from REM) • ST: dream - sleep tracker • wakes you up from REM sleep (closest to awake state) • AD: awake-daytime PSI dimensions: • • delusional thinking • perceptual distortions • cognitive disorganization • anhedonia: inability to experience pleasure • mania paranoia • • pairwise comparisons: if there is an interaction between two of the groups • overall, natural waking and sleep tracking did not differ • results: • overall, PSI was higher in sleeptrackers (statistically significant) • natural waking and sleep tracking were statistically the same —> overall, coming out of the state of ANY sleep had an effect on PSI (report more psychotic symptoms out of sleep state than wake state) • delusional thinking • ONLY sleep tracking greater than awake • perceptual distortions • both ST and NW greater than awake • most PSI in NW and ST are greater than awake, important differences in between sleep states • something about coming out of a dream state is more like a psychotic state than when you are awake • across several psychotic dimensions • “Slow wave sleep during a daytime nap i necessary for protection from subsequent interference and long-term retention” • research question: does sleep facilitate memory formation/consolidation? • does sleep have an active or a permissive role in this memory consolidation? • active role: sleep ACTUALLY helps you consolidate information • permissive role: when you’re awake you are distracted, and when you’re asleep there is no interference (so you do better on memory tests) • synaptic homeostasis hypothesis: when awake, start at baseline in the morning (synapses plastic) - with experience, synapses modified and circuitry strengthened • as you get more and more information, amount of plasticity of synapses decrease over course of the day until they are saturated - cannot store any more information • with sleep, synapses return to baseline • standard theory of consolidation: memory becomes strengthened over time • hypothesis: SWS facilitates memory formation • methods: behavioral intervention (2 psychological/behavioral variables) • independent variables: length of nap 7 Tuesday, March 8, 2016 • no nap • train, wake, test 1, train, test 2, 1 week interval, test 3 10 minute nap (no SWS - only get into stage 2) • • train, 10 minute nap, wake, test 1, train, test 2, 1 week interval, test 3 • 60 minute nap (all sleep stages) • train, 60 minute nap, wake, test 1, train, test 2, 1 week interval, test 3 • dependent variable: retention/memory • declarative memory: explicit (factual information) doesn’t really have a somatic variable - this variable is also behavioral • • training: paired words with sounds (audio clip for 2 seconds followed by the word, followed by both at the same time) • 36 pairs • exposed to these pairs until 75% criterion (75% correct) - exposure varied • test 1: recall of word associated with given sound interference: testing whether sleep is permissive or active • • interfered with ALL groups • paired new words with previous sounds (learning new associations with old tones) • trained up to 90% criterion - know that these new associations have been formed • test 2: testing for initial pairs AND newly learned pairs • test 3: after a week - tests long term memory results: • • learning was the same in all groups (expected - all had the same treatment to this point) • test 1: only statistical different between 60 minute nap and awake • interference learning: 60 minute nap did best (10 minute and awake not different) • test 2: significant effect between • 60 minute nap did better • short term: • 60 minute nap better than no nap • long term consolidation • 60 minute nap better than 10 minute nap AND awake • short nap had no effect over no nap • due to lack of interference?? • original difference: 60 nap > 10 nap > no nap • BUT when all given same interference condition - effect of interference is NOT the same in each group (suggests ACTIVE ROLE) • selectively has bigger effect on both napping groups • interferes the MOST in awake and 10 minute nap - LESS in longer nap • active role suggested by the fact that interference was less noticeable in longer naps - says that longer naps allow for better consolidation of memory Emotions • components: • feelings: subjective, internal state (different for everyone) • actions: evolutionary component (ex: attacking, defending, etc) • functional role of emotion • physiological arousal: somatic/autonomic responses 8 Tuesday, March 8, 2016 • motivational programs • folk psychology: stimulus —> perception/interpretation —> experience emotion (ex: fear) —> specific • autonomic arousal patterns (ex: heart racing, sweating, etc.) • autonomics responses caused by emotional experience • James-Lange theory • stimulus —> perception/interpretation —> specific pattern of autonomic arousal —> particular emotion experienced autonomic response is BEFORE emotion - experienced emotion is a result of the pattern • of autonomic arousal • each emotion must have specific pattern of arousal (source of criticism for this theory) • Cannon-Bard theory: • stimulus —> perception/interpretation —> GENERAL autonomic arousal AND particular emotional experience bodily response and emotional experience are simultaneous • • parallel processing • Schachter’s cognitive attribution model • stimulus —> perception/information —> stimulus AND context • stimulus —> general autonomic arousal —> particular emotional response —> feedback to perception and interpretation context —> particular emotional experience —> FEEDBACK to perception and • interpretation • study conducted where subjects injected with epinephrine • activates autonomic (sympathetic) nervous system • told some people - because they knew, they did not interpret bodily reaction in an emotional way • did not tell others - these attributed heart racing/sweating to emotions • one group with happy confederate • these people tended to report feeling happy • one group with angry confederate • tended to report feeling angry • context dictated emotional experience (reaction to epinephrine) • supports Schachter’s cognitive attribution model • are there a select number of emotional states?? or is it a spectrum?? • set number (about 8) of opposing emotions on orthogonal spectrum • BUT these emotions vary in intensity • ex: high intensity is loathing, medium is disgust, low is boredom • facial expressions: Darwin questioned whether universal or culturally determined • happiness tends to be almost completely agreed on throughout all groups • mostly agreed on in literate (both nonwestern and western) • in a study other than happiness, in isolated non-literate groups there is less agreement • in each culture, there is mediation by culture-specific display rules • there are universal expressions, but different cultures have different levels of acceptance for emotional display • facial expression physiology: • control of facial muscles by different cranial nerves • VII: facial nerve - controls superficial muscles (expression) • branches: • temporal 9 Tuesday, March 8, 2016 • zygomatic • buccal mandibular • • V: trigeminal - controls jaw muscles • facial muscles: • temporalis • frontalis • orbicularis oculi levator labii superioris • • facial feedback hypothesis • when you smile, brain interprets (via motor output of cranial nerves) type of expression • brain uses this information to make decisions about how you feel • if you feel sad, smile (forces brain to think you’re happier) • put a pencil between your teeth (to mimic smile) college students rated cartoons as funnier • • students who had pencil under the nose (to mimic sad face) thought comics were less funny • Botox flattens emotional experience • Papez circuit: • original circuit of emotion experience of emotion determined by activity in cingulate cortex and other cortical areas • • emotional expression governed by hypothalamus • cingulate projects to hippocampus which projects to hypothalamus (via fornix) • then goes to cortex • limbic system (McLane’s triune brain) • cingulate circuitry from thalamus, cingulate feeding back to hippocampus/mammillary bodies and amygdala • cholinergic nuclei in basal forebrain spread through cortex • sensory info to thalamus, processed in circuit (looking at emotional components) • brain regions involved in emotion • orbitofrontal region • anterior cingulate - unexpected/surprising stimuli • posterior cingulate • amygdala • insular cortex • are emotional patterns associated with same brain areas? NO • sadness: • increase in activity in anterior cingulate • decrease in posterior cingulate • increase in insula • increase in dorsal pons • happiness: • increase in posterior cingulate • decrease in anterior cingulate • increase in insula • fear: • increase in midbrain (important) • decrease in orbitofrontal • anger: 10 Tuesday, March 8, 2016 • increase in pons • increase in left anterior cingulate fear conditioning - common way to study emotion in lab • • conditioned stimulus: tone • unconditioned stimulus: electrical shock • animal trained to fear tone (associated with shock) - after pairing • blood pressure increases • freezes (motionless) 2 photon microscopy: • • engineer cells to have photosensitive response - fluoresce when excited • rat cortex exposed (in this study, frontal lobe) and covered with glass • excited cortex with light - able to see formation and elimination of dendritic spines • lots of controls: • tone only shock only • • unpaired • paired (result of learning) • results: after fear conditioning • NO difference in number of spines EXCEPT in the learning group • almost 2x increase of eliminated spines pruning took place in the frontal cortex • • no difference in spine formation • level of freezing increases with % spine elimination (positive correlation) • more spine elimination = more afraid • amygdala ONLY area in which lesions completely abolish fear conditioning • in limbic system, but only amygdala has this association • different nuclei • centromedial • central • basolateral • reciprocal connections with frontal lobe • can isolate all the components of fear conditioning based on connections within amygdala • pathway: • stimuli —> sensory organ —> thalamus • thalamus can go to high road or low road • high road —> sensory cortex/hippocampus —> amygdala • low road —> directly to amygdala (different nuclei) • projections from amygdala (these are all independent pathways - lesions in one allows others to still function) • central gray —> emotional behavior • severed connection eliminates emotional behavior BUT maintains autonomic and hormonal connections • lateral hypothalamus —> autonomic responses • bed nucleus to stria terminals —> hormonal responses • fear seems to be unique in that is has a specific area in the brain (not a similar area for happiness) • self-stimulation paradigm: pleasurable stimuli • way to study other components of emotion in rats • stick electrode in brain: if rat presses bar, neurons stimulated and nt released 11 Tuesday, March 8, 2016 • can put it anywhere - some found to be aversive, some like being stimulated • areas most enjoyed are associated with addiction able to see where rats like to be stimulated • • rats must “like” whatever stimulations they choose • circuitry in the brain - certain areas with electrodes that rats LOVE • nucleus accumbens (part of ventral striatum) - male rats will press bar until they die (ignore ALL other stimuli - females, food, etc) • reward circuitry mesolimbic (midbrain to limbic) dopamine system • • addiction areas • stimulation of ANYWHERE along this pathway is rewarding (especially nucleus accumbent) • we enjoy dopamine spritz (small amount) - pleasurable, rewarding • cocaine REALLY stimulates these areas - hijacks system to induce a lot of pleasure our brains have developed in a way to return to homeostasis • • increasing levels of dopamine result in brain counteracting this - will decrease the number of dopamine receptors • brain wants to stay at the same level - leads to drug tolerance • in the absence of stimulation, this system is hardly active at all - reason that former drug addicts have difficulty feeling pleasure areas: • • cerebellar nuclei • locus coeruleus • substantia nigra • ventral tegmental area • nucleus accumbens • medial forebrain bundle • basal forebrain • at the neural level, we can dissect emotion into component parts • dissociable systems • behavior • cognitive response • VTA is the origin of dopaminergic projections • PAG more modulatory • different emotions seem to be processed in different brain areas (slide 24) • reward aka seeking/expectancy: • VTA • lateral hypothalamus • PAG • nucleus accumbens • fear: • PAG • amygdala • panic: • dorsomedial thalamus • bed nucleus of stria terminals • PAG • anterior cingulate • happiness/play: 12 Tuesday, March 8, 2016 • dorsomedial thalamus • PAG parafascicular area • Stress • evolutionarily: system operates at a level that conserves energy • when we need to use reserves, we can • enhanced performance is costly, but available • responds well to acute stressors • our social systems put us under chronic stress, which we are not evolutionarily designed to handle • stressor: physiologically, anything that perturbs the system • body likes homeostasis - stress response returns us to homeostasis • HPA system • in response to stress, hypothalamus activates SNS to stimulate • adrenal medulla - releases epinephrine and norepinephrine (faster response) • neurocrine response: release of neurotransmitters through axons • • hypothalamus stimulates anterior pituitary to release hormones that cause adrenal cortex to release cortisol (slower response) • endocrine response relies on release of signaling molecules into bloodstream • slow pathway • neuroendocrine cell bodies in hypothalamus produce releasing and inhibiting hormones hormones released into hypophyseal artery (portal system), which connects to anterior • pituitary • releasing hormones: corticotropic releasing hormone (CRH) and thyroid releasing hormone (TRH) • cells in anterior pituitary release tropic hormones • ACTH - adrenotropic corticotropic hormone prolactin • • TSH - thyroid stimulating hormone • growth hormone • tropic hormones enter bloodstream and get to targets • adrenal cortex releases corticosteroids • thyroids release thyroid hormones fast pathway: • • neurons travel through spinal cord • activate sympathetic system, which activates adrenal gland • adrenal medulla releases epinephrine into circulation • study of stress response: parachute jumpers • able to dissociate anticipation of stress (psychological) vs actual physiological stress psychological component of stress response is VERY important • • how you interpret/process stress has huge impact on physiological stress • hormonal responses affect thyroid, adrenal gland, testes • parasympathetic responses affect heart, liver, intestines, bladder • inactivated in stress • sympathetic responses affects heart, spleen, adrenal gland, pancreas, intestines, liver 13 Tuesday, March 8, 2016 • activated in stress • before training: huge jump in cortisol with anticipation and after jump (first time) initially, a huge drop in testosterone • • after doing it many times • cortisol levels fall back to almost baseline • epinephrine stays above baseline after jump • norepinephrine seems to stay higher before (maybe to prepare) • growth hormone stays above baseline growth hormone decreased before jump, increases after jump • • study of stress response during transportation strike • measures epinephrine levels - elevated epinephrine with crowded train • in days before taking an exam, norepinephrine and epinephrine slowly increase until HUGE spike on exam day • De Quervain - 2000 trained subjects to memorize 60 nouns (recall test) • • one hour before test, half of subjects received cortisone tablet, half got placebo • later, took recall test • cortisone group recalled significantly FEWER words • cortisone release causes significant memory impairment • short term stress can be good, but long term can be detrimental (at least for memory) more excitable animals have higher expression of “strex” gene • • “adrenaline junkies” have less expression of these genes, so they want to reach the same levels as other people • everyone wants to reach same level, but some born with higher gene expression • individual differences in perception of stressors • experiment: 2 rats exposed to identical stressors (intermittent electrical shocks) • one rat gets signal (lets them know when signal will end) • this rat displayed much lower corticosterone response than the other • one gets nothing (no knowledge of duration) • displayed higher corticosterone - doesn’t know how long it will last • important psychological factors • predicability VERY important - not knowing duration of stressor potentiates stress response (better if you know duration) • loss of sense of control • outlets of frustration (ex: running decreases stress response) • adaptive components become problems if stress stays for long term • adaptive components: in SHORT TERM • mobilization of energy at cost of energy storage • increases heart/lung tone • suppression of digestion/growth/reproduction/immunity • analgesia • neural responses (altered cognition, sensory thresholds) • pathological issues (if stress becomes PROLONGED) • fatigue, muscle wasting • hypertension, ulcers • dwarfism • suppression of ovulation • impaired disease resistance • apathy 14 Tuesday, March 8, 2016 • neural degeneration • stress causes cortisol secretion cortisol secretion tends to destroy hippocampal neurons • • fewer hippocampal neurons leads to a DECREASE ability to shut down cortical secretion • hippocampus uses negative feedback, acts as brake to stop cortisol secretion • leads to more cortisol secretion…..cycle repeats • neurotoxic pathways • interaction of nervous system, immune system and endocrine system these all influence each other • • slide 11 cycles • 2006 Sheldon and Cohen experiment • somatic intervention • questionnaires to human subjects: • perceived life stress, life events, etc subjects exposed to 1 of 5 viruses via nasal inhalation (or control) known to cause upper • respiratory infections • after, quarantined for 5 days • measured levels of antibodies - immune response • those who had long term stressors (in questionnaires) significantly more likely to develop symptoms of cold/flu those with acute stressors unlikely to develop symptoms • • those with few stressors who REPORTED high stress levels ALSO significantly likely to develop symptoms • perceived stress can also decrease immune response • inflammatory cytokines operate as signaling molecules in nervous systems • neurons recognize them as neurotransmitters - affects brain activity • important in aging process - inflammaging (decreased cognitive function related to levels of inflammation) • stressors (social, microbes, toxins, impaired nutrition) • body defense system - ALL of these influence each other • immune system • genetic factors • endocrine factors • nervous system, memory/perception, coping and appraisal strategies Research Articles • Differential Immune System DNA Methylation and Cytokine Regulation in Post-Traumatic Stress Disorder • DNA methylation: adding a methyl group • way to measure DNA regulation • DNA neatly coiled around histones in order for gene to be expressed, have to physically expose portion of molecule which • can bind to promotor • experiential regulation AND inherited • usually decreases gene expression • epigenetic changes: don’t affect actual sequence of nucleotides, but alter expression of genes (methylation is an example) 15 Tuesday, March 8, 2016 • PTSD: due to exposure to traumatic events • symptoms: intrusive memories, thoughts and feelings hyperarousal • • anxiety • cytokines: signal in neurocrine system - act like neurotransmitters • not genes - actual molecules • CpG sites: bases that are in line with each other • hypothesis: exposure to traumatic events (childhood trauma or later in life) may cause epigenetic changes to DNA, which may alter behavior • DNA methylation may mediate persistent changes in the functioning of genes after chronic stress • childhood trauma OR high levels of lifetime cumulative stress will result in changes in DNA methylation • plasma cytokine levels will be associated with PTSD chronic stress changes immune dysregulation • • differentially methylated CpG sites over represented in genes related to immune function and inflammation • relationship between stress levels and development of PTSD • psychological stress may change the DNA methylation patterns (from immune dysregulation due to stress) methods: • • correlational study - no intervention • administered PTSD scale - people who are clinically trained asses the subjects • instrument administered by clinician • questionnaire asking about exposure to childhood trauma • took blood sample from periphery (not in the brain) • may or not be related to brain’s blood (due to BBB) • split into 4 groups based on PTSD and child abuse • PTSD patients vs. control group • measured total life stress (TLC) • results: • beta value: measure of methylated vs. un-methylated CpG sites • greater beta value indicates higher methylation • overall: PTSD patients have higher levels of global methylation in the genes of their peripheral blood • this technique is very touchy: amazing because you can look at so many genes, but so much data that it is VERY difficult to interpret • in this study - the ones examined demonstrated the largest changes • differently methylated in several areas - seems that the genes that showed the biggest changes in methylation have to do with stress/immune response • some go down in PTSD while some increase • translocated promotor region (TPR) decreased in methylation with PTSD • TPR interacts with glucocorticoid receptors (measures main stress hormone) • CLEC9A increased • associated with immunoreceptor (immune response) • ACP5 increased • phosphatase (removes phosphate groups) • stops short term plasticity • ANXA2 decreased 16 Tuesday, March 8, 2016 • TLR increases • related to stress total life stress plotted against methylation • • lowest levels of methylation associated with the highest life stress • TNF alpha: cytokine • stimulates HPA axis • pro-inflammatory response • increased with total life stress - inflammation increases with stress cytokine levels more associated with total life stress • • methylation levels more associated with PTSD • Brain response during visual emotional processing: an fMRI study of alexithymia • alexithymia: inability to recognize/describe emotions (issues in emotional processing) • process emotion differently, cannot understand different emotions • in 10% of general population previous studies have shown inconsistencies in brain areas associated with alexithymia • • hypothesis: altered function in anterior cingulate cortex implicated in alexithymia • methods: • behavioral intervention • subjected to emotional stimuli and measured brain activity • independent variable: nature of the emotional stimuli dependent variable: brain activity • • emotional stimuli: pictures (2 scales) • positive or negative • high or low intensity • only used females • some gene differentiation between male and females • now NIH has requirement that you use both genders unless there is a good justification • groups of 15 (high and low alexithymia) • scale measured Alexithymia (had to test 432 females to get the 30 subjects) • took people that tested very low and very high • also self-rates anxiety/depression questionnaires - tried to minimize levels of anxiety and depression (controlled for this) • used fMRI to monitor brain activity in: • ACC • mPFC • insula • temporal lobe • took a baseline • results: • with negative high intensity stimuli: • less activation in temporal, frontal and ACC with high-alexithymic • positive high intensity stimuli: • MORE activation in frontal, precentral and insular gyro with high-alexithymic • mostly associated with cortex • **increase in lentiform/putame** (different memory system - part of basal ganglia) • positive low intensity stimuli: • more bilateral activity in ACC with high alexithymic 17 Tuesday, March 8, 2016 • both high and low alexithymic subjects showed similar activation in these areas with neutral stimuli alexithymic group associated with increases of depression and anxiety • • very few changes in the activity of the limbic system (except ACC) with these differences • mostly cortical differences - people with alexithymia seem to have issues with cortical processing of the information that is processed in the limbic system • cortical interpretation (reported subjective feeling) amiss limbic components are assembling emotional stimuli, which seem to remain • unaffected • positive and negative are not the same!! interpretation involves different brain areas 18


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