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PSYC 220 Week 8 Notes

by: Lynde Wangler

PSYC 220 Week 8 Notes PSYC 220

Lynde Wangler
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These are week 8 notes.
Meghan Jones
Class Notes
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This 6 page Class Notes was uploaded by Lynde Wangler on Sunday March 6, 2016. The Class Notes belongs to PSYC 220 at University of North Carolina - Chapel Hill taught by Meghan Jones in Spring 2016. Since its upload, it has received 20 views. For similar materials see Biopsychology in Psychlogy at University of North Carolina - Chapel Hill.

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Date Created: 03/06/16
PSYC 220 Week 8 Chapter 8 (Voice Thread) Wakefulness and Sleep  Endogenous Rhythms: exogenous (sunlight, social influences, societal influences) vs. endogenous (circannual and circadian rhythms) stimuli controlling behavior o Circadian rhythms also exist for other behaviors – eating, urination, hormone secretion, metabolism, drug sensitivity, and mood  Setting the Biological Clock: o Time giver – Light, exercise, arousal, meals, and temperature o Jet lag and phase shifts o Shift work o Strong link to mood; depression o Stress?  Suprachiasmatic Nucleus: (of the hypothalamus) drives biological rhythm retinal ganglion cells feed the retinohypothalamic path which provides light into to the SCN (melanopsin is the photopigment used) o How does blindness affect biological clock?  Per and Tim – proteins that promote sleep and inactivity; produced in highest concentrations at night; pineal gland releases meatonin 2 or 3 hours before bed  Sleep as an Active Process State Brain Activity Responsiveness Duration Sleep Moderate Moderate Hours decrease decrease Coma Low level, remains Little to none Typically weeks, steady then death or recovery Vegetative state Alternation No awareness of Months or years; between sleep and surroundings, but 50% chance of low-level arousal autonomic regaining response to pain consciousness in first 6 months Minimally Alternation Occasional periods Months or years conscious (one between sleep and of comprehension level above VS) low-level arousal of surroundings Brain death none none Until life support is removed  Stages of Sleep: relaxed vs. awake o Alpha waves (8-12Hz); relaxed and awake o Stages 1 & 2 – brain activity decreases, irregular low voltage waves; Stage 2 – sleep spindles and K complex o Stages 3 & 4 – slow wave sleep; heart rate and brain activity decrease; slow large amplitude waves indicate highly synchronized neuronal activity  Rapid Eye Movement (REM) Sleep: marked by irregular, low voltage, fast waves (increased, asynchronous activity); PGO waves – high amplitude electrical potentials (pons, lateral geniculate, and occipital cortex); heart rate, breathing, and BP more variable o Body muscles are more relaxed in this stage than others; biological clock – amount of REM sleep is more related to time of day than amount of time that you have been sleeping  Brain Mechanisms of Sleeping and Waking: o GABAergic inhibition induces “sleep” at a local level o Pontomesencephalon induces wakefulness via acetylcholine and glutamate signals to hypothalamus, thalamus, and basal forebrain o Locus Coeruleus induces wakefulness via norepinephrine signals to cortical areas in response to meaningful events o Hypothalamus induces wakefulness via histamine release throughout the brain  Orexin/Hypocretin: from lateral and posterior nuclei of hypothalamus o Extend to basal forebrain, other areas o Necessary for staying awake o Normally levels rise throughout the day o Blocking orexin receptors induces drowsiness  Sleep Disorders: insomnia, sleep apnea, narcolepsy, periodic limb movement disorder, night terrors, and sleepwalking  Sleep and Energy Conservation: o Hypothesis – sleep evolved to conserve energy o Evidence for – virtually every species more efficient at some time of the day; body temp decreases by 1-2C; muscle activity decreases; sleep duration increased during food shortage o Nervous system can adapt to changing needs; some species of dolphins – don’t sleep for first couple of weeks after giving birth; migratory birds – hunt all day, fly at night  Sleep and Memory: neurons that fired during wakefulness fire during sleep; same patterns, but faster firing; amount of activity correlated with improvement in skill o Weeding out unused connections – weakening of synapses occurs during sleep; synapses that aren’t weakened stand out  Dreams: o Activation-Synthesis Hypothesis – brain’s effort to make sense of sparse and distorted information (sense of falling) o Clinico-Anatomical Hypothesis – when cortical activity is decreased, our thoughts from other brain areas are free to generate images without constraints (thinking under unusual conditions) Chapter 9 Internal Regulation  Homeostasis: physiological mechanisms maintain acidity, saltiness, water level, oxygenation, temperature, and energy availability within the body; homeostasis around a set point (a single value that the body works to maintain) through negative feedback mechanisms o Allostasis – homeostasis around an adjusted set point  Temperature Regulation: o Thermoregulation – basal metabolism (energy used to maintain constant body temperature); why would we want to maintain a constant (warm) body temperature?; ectothermic vs. endothermic; temperatures below freezing or above 109F are life-threatening  Mechanisms of Thermoregulation: Physiological – shivering, sweating, constriction/dilation of blood vessels, accelerated respiration  Brain Areas Important for Temperature Regulation: Preoptic area (POA) and anterior hypothalamus (AH)  Immune Function and Temperature: fever is adaptive change in the body’s temperature set point; Pathway of activation: leukocytes release small proteins called cytokines 1)attack infection, 2) stimulate release of prostaglandins from hypothalamus to induce fever Temperature receptors in the skin Temperature receptors in brain and other organs POA/AH  Infection immune response prostaglandins and histamine  POA/AH – controls shivering, sweating, heart rate, blood flow to skin, metabolism in brown adipose tissue, etc.  Water Regulation: o Osmotic Thirst – a drive for water that helps restore the normal state of osmotic pressure  Osmotic pressure – the tendency of water to flow across a semipermeable membrane from the area of low concentration to an area of high concentration to an area of high concentrations o Hypovolemic thirst – thirst based on volume, animal desires salty water (pure water would dilute body fluid further)  Osmotic Thirst: Set point for concentration of all solutes in mammalian body fluids is 0.15M; Osmotic thirst occurs when osmotic pressure drives water out of the cell; cells in the stomach detect high levels of sodium; neurons detect their own loss of water o Greater concentration of solutes outside the cell than inside water flows out of the cell, equalizing the solute concentration and shrinking the cell  Osmoreceptors – increase solute concentration of interstitial fluid causes osmoreceptors to lose water and shrink in size  change in firing rate of axon  Osmotic Thirst – osmoreceptors located around the third ventricle; OVLT – organum vasculosum laminae terminalis; SFO – subfornical organ; info from OVLT & SFO to hypothalamus paraventricular nucleus & supraoptic nucleus o Control vasopressin release from posterior pituitary o OVLT & SFO  Hypothalamus (PVN & SON) posterior pituitary  vasopressin (ADH) constricts blood vessels and enables kidney to reabsorb water from urine  Hypovolemic Thirst: loss of fluids via bleeding, diarrhea, or excessive sweating; need to restore lost salts, not just water; drop in extracellular volume detected by baroreceptors; no change in osmotic pressure (salts and ions are lost with the water)  SFO then sends signals o hypothalamus to realease more vasopressin and increase drinking  Sodium-Specific Hunger: animal with hypovolemic thirst increases its preference for slightly salty water (developes automatically when sodium reserves are low); aldosterone produced by adrenal glands in response to low sodium (causes kidneys, salivary and sweat glands to retain salt); aldosterone and angiotensin II (can activate taste receptors, nucleus of tractus solitarius (NTS), other salty appetite regions in brain Chapter 9 Internal Regulation Continued  Feast vs. Famine: redundant and complex homeostatic mechanisms guide hunger because we need to monitor and maintain a wide range of nutrients (20 amino acids, carbohydrates – sugars and starches, minerals, vitamins)  The Human Digestive System: o Carnivores – get all the vitamins they need from their prey o Herbivores and Omnivores – social learning; taste (sweet=good, salty and sour=sometimes, bitter=harmful, familiarity) o One trial taste aversion learning – taste is a very potent stimulus in Pavlovian conditioning procedures  Feeding Regulation – oral factors (chewing gum); tasteless diet (liquid diet study); taste-only diet (sham-feeding experiments)  Feeding Regulation: Short Term o Stomach distension is the first signal for short-term satiety (preventing nutrients from passing to the small intestine did not interfere with short-term feeding o Hormone release in the duodenum (OEA, CCK) o Glucose is the principal fuel for cells in the body o Insulin – promotes conversion of glucose into glycogen for short term storage; enables glucose to enter cells; signals satiety o Glucagon – promotes conversion of glycogen back to glucose o Surplus sugars are stores as lipids in adipose tissue  Feeding Regulation: High Insulin o High insulin levels that persist even when there is plenty of glucose entering cells prepare the body for hibernation; no glucagon to balance the use of glucose stores with intake – store much more than you need to such that the cells don’t get as much glucose as normal; can we really blame our autumn weight gain on the holidays?  Diabetes: o Type I – lack of insulin production o Type II – insensitivity to insulin  Feeding Regulation: o Leptin – produced by fat cells, signals that you have plenty of nutrition  Leptin sensitivity declines as a result of pregnancy and obesity o Ghrelin – synthesized and released by cells of the stomach, signals appetite o PYY 3-36 – synthesized and released by cells of the intestines, signals satiety  Hypothalamic Regulation of Feeding: o Arcuate nucleus (AR)  Hunger-motive neurons – NPY neurons  Satiety-motive neurons – POMC neurons o Paraventricular nucleus (PVN)  Inhibited by hunger neurons  Excited by satiety neurons o Lateral hypothalamus  Inhibited by PVN  Output increases feeding  Hypothalamic Regulation of Feeding: NPY neurons are anxiolytic! Less stress hunger will be inhibited ; GABA, NPY, and AgRP inhibitory signals (two kinds of neurons in the lateral nucleus of the hypothalamus); cortical output – attentional biases to food  Hunger Signals: o 1. Inhibitory signal from arcuate nucleus to the PVN o 2. Inhibiting the inhibitory signal from the PVN to the LH  Results in disinhibition  Think of this as the “ releasing the brake” example o 3. Increase in eating behavior (because you are hungry)  Satiety Signals: o 1. Excitatory signal from arcuate nucleus to the PVN o 2. Increase the inhibitory signal from the PVN to the LH  Results in inhibition of the LH o 3. Decrease in eating behavior (because you are NOT hungry)  Lateral Hypothalamus: many pathways o NTS (taste and salivation); Cerebral Cortex (ingestion & swallowing; taste, smell, sight of food); Pituitary gland (insulin production); autonomic (digestive secretions)  Hypothalamic Regulation of Feeding: o Ventromedial hypothalamus is linked to satiety; activity in this region reduces eating behavior; lesions in these region lead to more frequent meals and increased insulin production  Obesity: significant genetic contribution, heritability (Prader-Willi syndrome – high blood levels of ghrelin); obesity was once evolutionarily adaptive; diet and exercise o Other treatments: appetite control (leptin, cannabinoids, PYY 3-36), increased metabolic rate (thyroid hormones); inhibition of fat; reduced reward; gastric bypass surgery  Need to adjust set point  Obesity/Eating Disorders: Over-Activity in Brain Areas Relative to Addiction: activation abnormalities higher in Obesity/Eating Disorders (relative to addiction); Putamen, insula, hippocampus, and temporal cortices  Obesity: Changes in Reward Circuitry: decreased response to receiving a milkshake in caudate for obese subjects (compared to those who are lean); Decreased activation in the caudate is negatively correlated with BMI  Anorexia-Nervosa and Bulimia Nervosa: o Anorexia-nervosa: net consumption of very little food o Bulimia-nervosa: alternate between periods of overeating and strict dieting (net consumption more variable) o Body dysmorphic disorder o Social pressures…but can’t be the whole story


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