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Brain and Behavior LECTURE NOTES Part 2 - I got a 4.0 in the class

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University of Pittsburgh

Lecture 8 Berthold’s expt: (1849) - Demonstrated existence & function of hormones o Hormones: messenger molecules; chemicals released by endocrine glands into the bloodstream to circulate to a body target & effect it  Control reaction to stress & regulate many body processes o Glands: cell groups in the body that secrete hormones - Endocrine system: organized hierarchically. Hormones: - Secreted into B.S. - Operate over long distance - Operate over long temporal range (time) - Peptides/proteins, monoamines, steroids (steroids can pass through B.B.B.) Neurotransmitters: - Secreted @ neuronal synapses - Short distance (20 nm) - Short temporal range - Peptides, monoamines,A.A.’s, gases H’s & NT’s both use the same monoamines (noradrenaline, adrenaline, dopamine…) Production & release of hormones 1. Hypothalamus & Pituitary System 2. Autonomic N.S. 3. Local Mechanisms 1. H-P System: Stimuli –(nervous signaling)Hypothalamus-(releasing hormones)Pituitary gland – (Tropic Hormones) Target Endocrine Glands *thyroid gland, adrenal gland, gonads) – (hormones) Target organs & issues H-T gland: (More than 20 nuclei “accumulations” of gray matter) - Below thalamus - Controls behavior - Controls P-gland P- gland - Endocrine gland attached to bottom of the hypothalamus - Its secretions control the activities of many endocrine glands H-P connections H: produces releasing hormones (peptides which regulate the release of hormones from the anterior (front) pituitary) P: Posterior Pituitary (does NOT synthesize hormones) - Neuronal tissue; continuation of the Hypothalamus - Releases oxytocin &Anti-Diuretic hormone (ADH)  ^^oxytocin in men = ^^ monogamy & relations; good husband Anterior Pituitary - Glandular tissue; synthesizes various hormones Control of Hormone production: feedback loop - Feedback loops control activity of the H-T through the amount of hormone released A. Hypothalamus-(releasing hormones (+))Ant. Pit. –(Pituitary h’s (+)) **Target organs** hormones **Target organs** send feedback loop to Hypothalamus (allosteric binding perhaps?) 2. Autonomic Nervous System Stimuli –(Nervous signaling)ANS –(Nervous signaling) Target Endocrine glands (mostly adrenal gland)  target organs & tissues (previous arrow could be for bloodstream maybe) • ANS mostly responsible for adrenaline? - No hierarchy 3. Local Mechanisms *only need to know glucose example…rise in blood glucose  production & release of insulin by pancreas Chemical changes in the body  Endocrine gland –(hormones)Target tissues & organs  restore chemical imbalance Functional Class of Hormones - Homeostatic hormones - Sex Hormones - Stress Hormones Homeostatic Hormones: maintain body’s internal environment - Body temperature, blood pressure, blood levels of salt/glucose & oxygen. - Ex: insulin/glucagon maintain constant level of blood glucose (~80mg/100mL Blood) Diabetes = failure of the pancreas to secrete enough /or any insulin –Type I  Cells become resistant to insulin – Type II  Neuronal cells become resistant to insulin – Type III Insulin: lowers blood sugar by increasing glucose uptake in cells (released by pancreas) Glucagon: liver increases blood sugar by breaking down its stored Glycogen into Glucose for it to re-enter bloodstream (released by pancreas) Sex Hormones: define sexual appearance, behavior & development. - Estrogens (female) &Androgens (males) present in both sexes but in different amounts. - Produced in gonads…also in adrenal gland…??? Hypothalamo-pituitary GonadalAxis  Gonadotrophin-releasing Hormone  Lotropin  testosterone  Gonadotrophin-releasing Hormone  Follicle stimulating Hormone  Estradiol o Testosterone & Estradiol = 6’-6’-6’-5’structure…testosterone has O= at the end…Estradiol has OH-. Anabolic Steroids - Aclass of synthetic hormones related to the male sex hormone (testosterone) that has both muscle-building & masculinizing effects. - Health risks: o Body reduces production of testosterone  reduced male fertility o Increased aggression…“Roid Rage” o Increased risk of heart attack / stroke o Masculinization of female users Stress Hormones & response - Stressor: stimulus that challenges body’s homeostasis & triggers arousal - Stress hormones = produced by adrenal glands - Two response to stress—Fast Acting (adrenaline—fight/flight; increased HR, dialated air passages, increased blood glucose) AND Slow Acting (Cortisol- turns off all systems not immediately required to deal w/ stressor)  increases energy supply (turns off insulin production ^^ blood glucose) Adrenal Glands- endocrine glands which sit @ top of kidneys  2 parts: Cortex (outer) & medulla (inner) Hormones = corticosteroids (cortisol); androgens Hypothalamo-PituitaryAdrenalAxis • H-P –(corticotropin releasing hormone) • Pituitary gland –(corticotropin) • Cortex of adrenal gland –(cortisol) • Target organs & tissues Activation byANS • Sympathetic Nervous system –(Noradrenaline (NT)) • Medulla of adrenal gland –(adrenaline (epinephrine)) • Target organs & tissues Ending a Stress response (S.R.) - Normally stress responses = brief - Stress responses turned on/off in brain Sapolsky (2005): Hippocampus involved in turning off S.R. • HC = high density of cortisol receptors, & has axons that project to the H-T • Too much cortisol will damage neurons in HC  Studies on caged vervet monkeys • Vicious cycle w/ prolonged stress, cortisol levels, & hippocampal functioning PTSD: caused by physiological arousal symptoms related to recurring memories & dreams related to a traumatic event – for months and years after the event.—usual diagnosis if symptoms persist for > 1 week Fear response regulated by:  Amygdala  Hippocampus • PTSD  shrunk hippocampus Lecture # 9 Neurobiology of motivation & emotion - Hypothalamus - Limbic System o Amygdala o Cingulate cortex o Hippocampus - Frontal Lobe - Mesolimbic Pathway H.T.: involved in generating behavior - electrical stimulation of different HT nuclei goal-directed behaviors such as:  eating/drinking  digging  displaying fear Habits are indistinguishable from  predatory or attack behavior normally-occurring behaviors  reproductive behavior Organization of L.S. Main:Amygdala, Cingulate Cortex, & Hippocampus - connections w/ P.F. Cortex, sensory association cortex, thalamus, and H.T. Amygdala: almond-shaped collection of nuclei, located w/in L.S. - role in emotional/motivated behaviors o stimulation makes patients  fearful/anxious o “ “ can induce eating/drinking - Receives input from all sensory systems - InfluencesAutonomic & hormonal responses via connections w/ H.T. - Influences Conscious awareness of the consequences of events and objects via connections w/ P.F. Cortex The Frontal Lobes: 3 main regions - Motor Cortex o Controls fine movements - Premotor Cortex o Selection of appropriate movement sequences - Prefrontal Cortex *(very impt.)* o Anterior part of the frontal cortex Functions:  Planning complex behaviors  Decision making  Organizing social behavior Damage to PF C – severe effects on soc. & emot. Behavior  Inability to experience & express own emotions/ recognize emotional expression of others  Apathy and Loss of initiative or drive  Inability to plan/ organize poor decision making Behavior = Regulatory (homeostatic) and Non-regulatory (non-homeostatic purposes) Regulatory Behavior: motivated to meet needs of animal controlled by homeostatic mechanisms involving the H.T. Ex: Internal Body Temp, eating/drinking, salt consumption, waste elim. Controlling eating: The Digestive system Goal: to gain nutrients (AA’s, lipids, glucose) • Hormones: cholecystokinin, insulin, growth hormone, etc. Hypothalamus Aphagia: failure to eat; maybe due to motor difficulties, especially w/ swallowing; observed following lesions to lateral HT Hyperphagia: eating too much (lesions to Ventromedial HT, or paraventricular nucleus of the H.T.)…..stomach detachment? Cognitive Factors • Amygdala o Projects to HT; damage alters food pref./ abolishes taste- aversion • Inferior PF cortex o Receives input from olfactory bulb o damage may  decreased eating because of diminished sensory responses to food odor/ perhaps taste. Eating disorders entail being over/underweight Obesity: excessive accumulation of body fat Anorexia Nervosa: exaggerated concern w/ being thin  to inadequate food intake & often excessive exercising; can lead to severe weight loss & even starvation Non-regulatory Behavior: strongly influenced by external stimuli  behavior unnecessary to meet the basic survival needs of the animal  not controlled by homeostatic mechanisms  most involve the frontal lobes > then HT ex: sexual behavior, parental behavior, aggression, food preference, curiosity, & reading Control of Sexual Behavior: hormonal effects on Brain Organizing effects of Sex Hormones - sexual dimorphism o differential development of brain areas in 2 sexes o Influenced by gonadal hormones (testosterone, estradiol) Activating Effects of Sex Hormones Adult female sexual behavior varies across estrous/menstrual cycle - In humans, sexual desire depends on gonadal hormone level - In non-humans mammals: estrogen levels ~ sexual receptivity - Rats: high estrogen also assoc. w/ ^^ dendritic spines on H.C. neurons - In adult males- testosterone levels influence motivation to seek sexual behavior & the production of copulatory behavior o Recent studies: in men sexual desire depends on the level of both estrogen & testosterone HT – controls sexual behaviors - Ventromedial controls female mating posture (lordosis) - Preoptic area of Medial HT controls copulatory behavior in males Amygdala: controls sexual motivation in males & possibly females Cognitive Influences on Sexual Behavior: - Cortex must have role on Sex. B in addition to the amygdala & HT but is poorly understood - Damage to Frontal lobes can  loss of sex behavioral inhibition or libido (sex. Interest) Lecture 10 Reward = positive reinforcement of behavior Behavioral model: intracranial self-stimulation Neuroanatomy of Reward Ventral TegmentalArea (VTA) (accumulation of neuronal cells)ect to the: - NucleusAccumbens (NAcc),Amygdala, HC, and PF cortex Mesolimbic Pathway: VTA NAcc********* NT: Dopamine - Evidence that ML system is involved in reward o Dopamine released in self-stimulation  Olds and Miller expt. (1954)  Rats will press a bar to self-administer electrical stimulation to specific sites in the brain (intracranial self-stimulation o Drugs that enhance dopamine release ^^^ self-stimulation, whereas drugs that decrease dopamine decrease self-stimulation o Dop. Levels ^^^ when animals mate & feed o Highly addictive drugs (nicotine/cocaine) increase dopamine levels in NAcc Reward: Wanting & Liking - two independent processes: wanting (incentive) and liking (evaluation of pleasure) o usually occur together but not always the case o Berridge (2009): wanting/liking have separable neural systems in NAcc  Wanting  involves dopamines  Liking  involves opioid & benzodiazepine-GABA NAcc Zones Sucrose = sweet taste quinine = bitter taste Drive (Arousal) - can be aroused w/out motivation but cannot be motivated w/out aroused = hypothetical state that motivates org. to engage in particular behavior. - Operationally defined by sensory alterness, motor activity & emotional reactivity, & the driving force behind behavior of all organisms according to their responses to stimuli • “Drive theories” assume brain is storing energy for certain behavior o “Flush” model- Separate energy stores for separate behaviors, are drained for particular behaviors once started Yerkes- Dodson Law Performance ^^^ to a certain point as arousal increases • Peak level @~ medium arousal (Stress?) o Optimum performance on easy task occurs @ higher level of arousal than on more difficult task Neurobiology of Drives: - Researchers unable to link drives/ brain activity - Behavioral change correlates w/changes in hormones & cellular activity o Cortisol = ^^ blood glucose level (is good) Ex: man’s frequency of sex = correlated w/ levels of androgens (male H’s.) - Hormones  sig. impact on vigilance & cognitive performance  Follows Y-D curve Visceral response: HT (hormones &ANS)…..^^^ H.R. Expressive heaviors: (facial expressions)….frontal lobes Subjective feelings (fear)….Amygdala & parts of frontal lobes (P.F. cortex) Conscious experience (thoughts about exp.)…cerebral cortex, sometimes difficult to define Kluver-Bucy Syndrome: behavioral syndrome  loss of fear, & hypersexuality, (in monkeys, includes indiscriminate eating habits- inedible object eating…) - Results from bilateral injury to amygdala - Tendency to examine objects by mouth - Attempted copulation w/ other species & ^ homosexual & autoerotic behavior Neurobiology of Emotion: PF cortex ( controls emotional behavior) - Experiencing emotions - Ability to recognize E’s in other people Damage to PF cortex  severe social and emotional behavioral effects Lobotomy- cut connections to/from PF cortex • Used to treat psychiatric conditions (1935-1950’s) • Controversial w/ serious side effects •  severe emotional changes James-Lange Theory: Stimulus  ANS Arousal [visceral response (amygdala)]  brain interprets it as emotion Visceral experience = muscular tension, a rise in HR, perspiration & dryness of mouth…labeled by brain as an emotional state. Two-Factor Theory: stimulus  both arousal & cognitive response  both lead to emotion Evidence: “Suproxin Expt” (1962) men given epinephrine- produced either happy/angry emotions w/confederate High Bridge expt: men crossing scary bridge were more attracted to women on the other side than those who crossed minor bridge - Theories - Visceral response - Internal organs associated w/ emotional response Love: oxytocin,ADH, dopamine, serotonin, testosterone - Brain Areas: activated (anterior cingulate cortex, HC, NAcc, & HT)  Deactivated: amygdala, Frontal cortex, PF cortex Lecture 11 – Biological rhythms. Sleep Biorhythm – timing mechanism to initiate various biological processes Period- time dur. of cycle of activity - Linked to cycle of days/seasons o Produced by Earth’s rotation/revolution around sun. 1. Circannual rhythm a. Yearly (birds migrate) b. Animals living near Earth’s poles = more affected by seasonal changes than those at equator 2. Circadian a. Daily b. Human behavior = governed more by daily cycles than by seasonal cycles Biological clock  “ rhythms  Time givers (external cues)….day/night or seasonal changes B.C.’s – endogenous (control comes from w/in) - movements of plant leaves w/out Ext. cues - free – running rhythms - System that times behavior - allows anticipation before event * Birds migrate before cold temps B.C.’s = first shown in plants - day shamrock leaves = ^ - night “ “ = V - plants isolated from dairy light/ dark cues & from temperature cues, but rhythmic movements continued Free-Running Rhythms (1960’s Aschoff / Weber) - People in bunker w/out outside ex. Cues o Sleep-wake cycle shifts ~1 hr/day How to study in Noct. Vs. Diurnal: Free-running periods- periods w/out e.c.’s (independent of e.c.’s) Hamsters w/ running wheel: constant darkness, FR = < 24 hours Constant light  FR longer than 24 hrs Sparrows – dark = FR> 24 hrs  Light = FR < 24 hrs Animals expand / contract their sleeping periods as the sleep-related lighting period – light for hamsters and dark for sparrows – expands and contracts. Zeitgeber – environmental event that entrains Biol. Rhythms “a time giver”, external light resets B- clock Entrainment- “resetting” internal bio-clock. Light Pollution: artificial lighting disrupts circadian rhythms & accounts for great deal of inconsistent behavior associated w/ accidents, daytime fatigue, & fluctuations in emotional states. SAD (seasonal affective disorder) – mood disorder similar to depression based on seasonal change = winter dep. Or summer dep. Sympytoms: dec. energy, ^^ sleep, ^^ appetite, ^^ carb craving, difficulty concentrating, dec. sex drive Treatments: light therapy, antidepressants, melatonin, cognitive-behavioral therapy Jet- Lag: Fatigue/ disorientation from rapid travel through time zones or an exposure to a changed light-dark cycle. **suprachiasmatic nucleus (SCN)** “supra” = above - Main pacemaker of circadian rhythms - Located in HT, just above optic chiasm (crossing of optic nerves) Evidence: Martin/ colleagues - Neurons in SCN maintain rhythmic electrical activity even when all pathways in/out of SCN = cut - SCN neurons = ^^ active during light period than dark period o Woman w/ tumor involving SCN = circadian rhythms were abolished o Conclusion: endogenous rhythm = not learned Pacemaking Circadian Rhythms - Light entrains C-R’s o Retino-hypo-thalamic pathway – neural route from subset of cone receptors (in retina) to SCN of HT; allows light to entrain the rhythmic activity of the SCN - SCN pacemakers drive # of dependent oscillators (“slave oscilators”) each of which controls the rhythmic occurrence of 1 behavior (e.g. BT) Outputs of SCN (pacemaker): HTPituitaryadrenal gland cortisol rhythmic changes in appetite, motor activity ANS multiple effects (e.g. rhythmic changes in body temp)  pineal gland (“third eye”) melatonin decreases motor activity, induces fatigue, lowers BT Melatonin (dietary supplement) - Hormone secreted by pineal gland during dark phase of D-N cycle - Light suppresses secretion o Principally blue light, around 460-480 nm o Regulates the sleep-wake cycle by chemically causing drowsiness & lowering body temperature o Controlled by the SCN Light retino-hypo-thalamic tract  SCN  Superior Cervical ganglion  Pineal gland Lecture 12 - Variation in behavior - Sleep more when young - Most ppl sleep 7-8 hours/night - Some much less Sleep need vs. Sleep Urge Sleep urge decreases mostly except for midday where it increases slightly around 2 pm Measuring sleep in Lab - Polygraph used to measure electrical activity of brain/body 1. Electroencephalogram (EEG) o Record brain-wave activity 2. Electromyogram (EMG) o Record muscle activity (facial usually) 3. Electroculogram (EOG) o Record of eye movements Usually placed on four main brain lobes EEography = recording of electrical brain activity through electrodes on surface of scalp. Used to study brain rhytms in active states/ during sleep, as well as to diagnose epilepsy. Gama rhythm (active thought) – Decrease associated w/ cog. Decline o X-modal sensory processing (30 Hz  100 Hz)  Dec. sig w/ people who have skitzophrenia Beta rhythm (alter/ walking state) – 13 30Hz Alpha rhythm (relaxed/reflective state) – 813 Hz…extremely regular brain rhythm - Therapy for anxiety- 10 Hz alpha rhythm stimulation Theta rhythm (drowsy state)- (4-8 Hz) Drowsy / meditative Delta rhythm (sleeping/dreamy state)-(0.5  4 Hz) pattern associated w/ deep sleep Test Q: what brain rhythm when _______? Sleep = REM sleep & non-REM sleep - Rapid eye movement - 1953, Aserinsky & Kleitman (wake people during sleep w/REM’s; could retell dreams) - Vivid dreams occur during REM sleep - Atonia (No turning over or kicking or anything) o No tone; condition of complete Muscle inactivity produced by the inhibition of motor neurons Non-REM sleep= large range of activities take place Ex: BT decrease, ^^ growth H release - Dreaming does occur in non-rem sleep, but dreams = not as vivid as in REM sleep o sleep walking o sleep talking o night terrors * know EEG, EMG & EOG changes during phases.Awake, REM, non-REM* Stage ½: Light, non-
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