Biopsychology Exam 3 Fall 2024 PDF
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Uploaded by RealizableGhost
University of Pittsburgh
2024
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This document contains material related to Biopsychology, focusing on Hunger and Eating, and the digestion process. It details the different phases of energy metabolism and storage.
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1/7/24 1 Hunger and Eating Digestion ○ Breaking down foods and absorbing its nutrients ○ Purpose of eating is to provide the body with molecular building blocks and energy Parotid glan...
1/7/24 1 Hunger and Eating Digestion ○ Breaking down foods and absorbing its nutrients ○ Purpose of eating is to provide the body with molecular building blocks and energy Parotid gland secretes enzymes that help break down starches & carbs Salivary gland provides lubrication for the chewing process - breaks and separates food in the mouth Gastrointestinal tract process ○ Chewing breaks up food and mixes it with saliva ○ Saliva lubricates food and begins its digestion ○ Swallowing moves food and drink down the esophagus to the stomach ○ Primary function of the stomach → storage reservoir The hydrochloric acid in the stomach breaks down food into small particles Pepsin begins the process of breaking down protein molecule to amino acids ○ Stomach gradually empties its contents through the pyloric sphincter into the duodenum & jejunum, the upper portion of the intestine where most of absorption occurs ○ Digestive enzymes in the duodenum, gallbladder, and pancreas break down protein molecules to amino acids, and starch and complex sugars to simple sugars Simple sugars and amino acids pass through the duodenum wall into the bloodstream and are carried to the liver Fats are emulsified by bile (made by the liver, stored in the gallbladder, & released into the duodenum) Cannot pass through the duodenum wall and is carried by small ducts in wall into the lymphatic system ○ Most of the remaining water and electrolytes are absorbed from the waste in the large intestine - remainder is ejected from the anus Energy delivery ○ Lipids & fatty acids ○ Amino acids ○ Glucose Energy storage ○ Triglyceride (2) In adipose (fatty) tissue About 85% Second storage tapped for energy Fatty acids → ketones → energy → glucose 1 gram stores twice as much energy as glycogen Don’t attract water ○ Protein (3) In muscle tissue About 14.5% Third storage tapped for energy ○ Glycogen (1) In liver About 0.5% First storage tapped for energy Attracts water Converted into glucose by glucagon when the body needs it Quick conversion 3 phases of energy metabolism ○ Cephalic phase Preprepatory phase initiated by interaction with food (sight, smell, expectation) Insulin levels high, glucagon levels low Promotes Utilization of blood glucose as a source of energy Conversion of excess glucose to glycogen and fat Conversion of amino acids to proteins Storage of glycogen in liver and muscle, fat in adipose tissue, and protein in muscle Inhibits Conversion of glycogen, fat, and protein into directly utilizable fuels – glucose, free fatty acids, ketones ○ Absorptive phase Nutrients from a meal meeting the body’s immediate energy requirements, with excess being stored Insulin levels high, glucagon levels low Promotes Utilization of blood glucose as a source of energy Conversion of excess glucose to glycogen and fat Conversion of amino acids to proteins Storage of glycogen in liver and muscle, fat in adipose tissue, and protein in muscle Inhibits Conversion of glycogen, fat, and protein into directly utilizable fuels – glucose, free fatty acids, ketones ○ Fasting phase Energy being withdrawn from stores to meet the body’s immediate needs Glucagon levels high, insulin levels low Promotes Conversion of fats to free fatty acids and the utilization of it as an energy source C onversion of glycogen to glucose, free fatty acids to ketones, and proteins to glucose Inhibits Utilization of glucose by the body, but not the brain Conversion of glucose to glycogen and fat, and amino acids to protein Storage of fat in adipose tissue What we eat ○ Evolution of tastes Typically prefer sweet, fatty, and salty foods In nature, sweet and fatty foods tend to be higher in nutrient value and energy than less sweet/fatty foods Salty foods are high in sodium and needed for electrolyte balance in the body Bitter tastes are not favored because they are generally associated with toxins and spoilage ○ Modeling of food preferences May learn to prefer foods eaten by others Infants are found to prefer flavors in breast milk & on breath of others (primarily seen in animals) ○ Vitamins and minerals Prefer foods that are good sources of vitamins and minerals, especially when there is a deficiency When we eat ○ Pre-meal hunger Initiates a cephalic phase shift - bodies adapt to eating on a schedule - related to circadian rhythm ○ Conditioning of hunger Cues in the environment are associated with eating - trigger cephalic phase Hunger peptide ○ Ghrelin Primarily produced and released by the stomach in response to signal from duodenum (when empty) Lesser amounts produced by duodenum & pancreas Levels increase during fasting (i.e. highest before meal) Results in perception of hunger Stimulates appetite Levels decrease during meal and are lowest after meal - depends on size and nutrient value ○ Neuropeptide Y Released by neurons in the hypothalamus The arcuate nucleus Appears to increase appetite and preference for carbs P otent stimulator of eating behavior Glucose-sensitive cells in medulla activate NPY neurons Glucoprivation (low levels of glucose) = increased NPY How much we eat ○ Satiety signals Food in gut Glucose in blood Volume of blood (Cannon & Washburn, 1912) Nutritive density food ○ Appetizer effect and satiety Small amount of food consumed prior to main meal Triggers absorptive phase & hunger You eat more when you eat an appetizer ○ Social factors and satiety People eat more (60%) when eating with others Less seen in females as compared to males ○ Sensory specific satiety Experience less pleasure and hunger when eating begins Positive incentive value → how pleasurable a taste is Within 30 mins the positive incentive value decreases for all foods available at the time Short term - in the moment Long term - whether specific food consumption continues Foods it doesn’t effect as much → rice, bread, potatoes, greens in a salad, sweets Encourages cafeteria diet (different types of food over periods of time) Allows us to get the nutrients we need with a varied diet When rodents are given a cafeteria diet, they are shown to eat more and gain more weight than normal - when given the same thing to eat all the time, rodents maintained a consistent weight and did not overeat Satiety peptide ○ Cholecystokinin (CCK) Secreted by upper small intestine (duodenum) Secreted in response to fats & amino acids in duodenum Stimulates gallbladder contraction to release bile Stimulates pancreas to release digestive enzymes Contracts pyloric sphincter (slows stomach emptying) Decreases hunger ○ Peptide YY In absorptive phase Secreted by cells in ileum (last section of small intestine) and colon Secreted in response to fat and protein presence Secretion is proportionate to the number of calories in food (consumed) More calories, higher response Slows gastric motility - increases water & electrolyte absorption by colon Decreases eating ○ Leptin Secreted by subcutaneous adipose cells (under the skin) Larger cells lead to more leptin release, vice versa Receptors found in brain (arcuate nucleus) Hyperpolarizes neuropeptide Y neurons - inhibits release of NPY Decreases food intake (eating) Increases metabolic rate Increases temperature and activity level Inhibits insulin synthesis and release Reduces the amount of orexin released Higher levels lead to lower sensitivity in neurons - seems to shut off the satiety mechanism Serotonin & satiety ○ Appears to increase short-term satiety associated with a meal ○ Serotonin agonists consistently reduced food intake in rats Resisted attraction of highly palatable diet Resisted urge to eat high calorie food Reduced amount of food consumed during meal Associated with shift in food preference away from fatty foods Similar effects seen in humans Fenfluramine and dexfenfluramine Serotonin has inhibitory effect on NPY receptors Set point theories ○ Premise Most people attribute motivation to eat with the presence of an energy deficit Belief that we eat to bring energy resources back up to an optimal level - energy set point ○ Glucostatic set point theory - negative feedback mechanism Hunger waxes and wanes as a function of blood glucose levels Hunger increases when glucose levels are low - eating restores glucose levels, thus reducing hunger ○ Lipstatic set point theory - negative feedback mechanism When fat stores are depleted, hunger increases to restore energy reserves - when fat stores are sufficient, hunger decreases Positive incentive theory ○ Premise Animals and humans are drawn to eating by the anticipated pleasure of the eating experience (positive incentive value of eating) Degree of hunger felt at any given point in time is dependent on all the factors that affect the incentive value of eating Settling point model ○ Premise Weight tend to drift around natural ‘settling’ point Settling point → level that the various factors that affect body weight reach equilibrium ○ *** Body weight tends to remain relatively constant in many adult animals over time Settling point theory helps to account for higher gains in weight during the adult years Weight that is less likely to come back off later because of the newly established state of homeostasis If diets are maintained, body weight eventually stabilizes at a new level Weight loss occurs rapidly at beginning of diet As weight declines, the amount of energy ‘leakage’ is automatically reduced which reduces the rate of weight loss Gradually, the reduced rate of intake is matched by the reduced energy output and a new settling point is achieved When the diet is terminated, weight gain is rapid because of the high incentive value of food and the low level of energy leakage As weight accumulates, the incentive value of food gradually decreases and the energy leakage increases until the original setting point is regained Brain mechanisms ○ Original/old view Ventromedial hypothalamus (VMH) Satiety center Stimulation resulted in aphasia Lesions resulted in ○ Hyperphagia ○ Increased meal frequency ○ High insulin levels Lateral hypothalamus (LH) Feeding center Stimulation resulted in increased eating (hyperphasia) and drinking (hyperdipsia) Lesions resulted in ○ Aphasia ○ Adipsia ○ Less arousal ○ Less movement ○ New research Lateral hypothalamus Melanin-concentrating hormone Orexin Stimulate/increase appetite Increase food intake behavior during meal Decrease metabolic rate Increase and preserve body energy stores Food deprivation results in increase of MCH & orexin Arcuate nucleus NPY and AgRP neurons produce neuropeptide Y and agouti-related peptide Neuropeptide Y stimulates orexin and melanin-concentrating hormone release from LH AgRP release activated by calorie deficiency AgRP inhibits satiety melanocortin 4 receptor (MC4R) neurons in the paraventricular nucleus of hypothalamus NPY & AgRP neurons have receptors for ○ Ghrelin (from stomach) Increase ghrelin = increase NPY ○ Leptin (from adipose tissue) Increase leptin = decrease NPY & AgRP Decrease orexin Increase alpha-melanocyte-stimulating hormone ○ Peptide YY (from ileum) Increase peptide YY = decrease NPY ○ Insulin (from pancreas) Increase insulin = decrease NPY 1/14/24 1 Learning & Memory Learning ○ Process by which experiences change our nervous system and change our behavior as a result - relatively permanent ○ Excludes behavioral changes resulting from sensory adaptation or fatigue Memory ○ Nervous system changes retained over time and how the changes are expressed (recall) ○ Types Sensory Short-term/working Long-term ○ Explicit Intentional recall of facts and events Medial temporal lobe Episodic Memories of specific events or personal experiences Semantic Memories of general facts or info ○ Implicit Unconscious memory processes - doesn’t require recall Associative conditioning Emotional ○ Amygdala Somatic ○ Cerebellum Procedural Striatum Priming Sensory cortex Non associative - habitualization, sensitization Reflex pathways General stages of memory ○ Acquisition Incoming information Sensory buffers ○ Encoding ○ Storage Short-term Consolidation to long-term Long-term can lead back to working Working Both short and long-term can lead to a loss of information ○ Retrieval Case of H.M. ○ Bilateral medial temporal lobectomy Removal of medial temporal lobes (MTL) bilaterally to alleviate severe epilepsy (1953) Hippocampus Amygdala Rhinal cortical areas Seizures significantly reduced Only patient to receive the treatment After surgery Intellect was above average ○ IQ improved from 104 to 118 points Normal perceptual and motor abilities Well-adjusted individual Poor memory abilities ○ Retrograde amnesia approx. 2 years before surgery ○ Profound anterograde amnesia Abilities Remember list of 6-7 digits ○ Digit-span + 1 test ○ Normal range in performance Tap sequence of 5 blocks ○ Block-tapping memory span test ○ Normal range in performance Relatively intact short-term memory if info was rehearsed Brenda Milner (1965) - “forgetting occurred immediately after the patient’s focus shifted Learned new behavioral skills Mirror-drawing task Improved with training sessions ○ Normal sensory-motor learning No conscious recollection of ever performing it before Showed normal priming ○ More likely to use a word if recently heard Repetition priming test No conscious recollection of the words on the original list Memory consolidation ○ Standard consolidation theory Squire & Alvarez (1995) Memories temporarily stored in hippocampus Later transferred to more stable system ○ Multiple-trace theory Nadel & Moscovitch (1997) Hippocampus and other structures store memories as they occur New similar experience, new engram Linked to original engram Synaptic mechanisms of learning & memory ○ Donald Hebb (1949) If a synapse is repeatedly activated at the same time a postsynaptic neuron fires, changes in the structure or chemistry of the synapse will strengthen it ○ Long-term potentiation (LTP) Synapses are effectively made stronger by repeated stimulation ○ Consistent with the synaptic changes hypothesized by Hebb LTP can last for many weeks LTP only occurs if pre-synaptic firing is soon followed by postsynaptic firing Induction of LTP ○ Synaptic strengthening depends on Depolarization of presynaptic membrane Simultaneous depolarization of the postsynaptic membrane ○ D epolarization of a neuron doesn’t strengthen all synapses, only those that are active at the time of depolarization Strengthening synapses ○ Action potential reaches terminal button of strong synapses - produces strong EPSP in pyramidal cell Depolarization is sufficient to trigger action potential in axon of pyramidal cell Dendritic spine washes back along dendrite - primes NMDA receptors in dendritic spines Action potential reaches terminal button - glutamate is released LTP - synapse is strengthened Backwash of depolarization occurs in these cells Induction of LTP in CA1 field ○ Stimulation of depolarization of presynaptic and postsynaptic membrane (glutamate) ○ Involves AMPA (found all over the nervous system) and NMDA receptors ○ Requires Na and Ca influx ○ Glutamate binds to AMPA receptors, opening sodium channels (depolarization) ○ Mg blocks NMDA receptor calcium channels If a molecule of glutamate binds with the NMDA receptor, the calcium channel cannot open because the Mg ion blocks the channel ○ Sufficient depolarization pushes Mg out, allowing Ca influx if glutamate binds to receptor (open channel) Depolarization of the membrane evicts the Mg ion and unblocks the channel - glutamate is able to open the ion channel and permit the entry of Ca ions Entry of CA ions activated enzymes - initiates LTP ○ AMPA receptors move into spine ○ Increased number of AMPA receptors strengthens synapse ○ AMPA receptors from interior of cell replace those moved into spine Dentate gyrus ○ Part of hippocampal formation ○ In medial temporal lobe ○ Helps the formation of episodic memories and the exploration of new environments ○ Potential to generate new neurons → adult neurogenesis CA3 field ○ In the Cornu Ammonis ○ Receives input from the dentate gyrus through mossy fibers ○ Involved in memory processes - encoding and retrieving spatial representations and episodic memories ○ Rich internal connectivity ○ Helps generate synchronous neural activity ○ P resynaptic neuron releases neurotransmitters into the synaptic cleft - bind to receptors on the postsynaptic neuron Postsynaptic neuron has a limited number of neurotransmitter receptors Small amount of calcium enters the cell and triggers baseline synaptic activity ○ Repeated activity of the presynaptic neuron leads to LTP induction More neurotransmitter-filled vesicles are released into the synaptic cleft High frequency stimulation results in more significant calcium entry into the postsynaptic neuron - activates intracellular signaling pathways - critical in initiating LTP Molecular changes enhance the efficiency of synaptic transmission ○ LTP leads to long-lasting increases in synaptic strength Postsynaptic neuron has a greater number of receptors - sensitive to neurotransmitter release Presynaptic neuron releases more neurotransmitters Calcium helps maintain the enhanced synaptic connection ○ Graph Shows electrical activity of the postsynaptic neuron overtime Baseline response represents normal synaptic transmission After LTP → much larger response = enhanced synaptic efficiacy Maintenance & expression of LTP ○ How are presynaptic and postsynaptic changes coordinated? ○ LTP may be involved in presynaptic changes (i.e. increasing glutamate levels) ○ Nitric oxide Synthesized in postsynaptic neurons in response to calcium influx - may diffuse back across gap to presynaptic neurons Memory storage ○ Each memory is stored diffusely throughout the crane structures that were involved in its formation ○ Hippocampus Spatial location - many neurons are place cells Explicit memory consolidation ○ Rhinal cortex - object recognition (semantic memory) ○ Mediodorsal nucleus - explicit memory ○ Damage to a variety of structures results in memory deficits ○ Inferotemporal cortex Visual perception of objects Changes in activity seen with visual recall ○ Prefrontal cortex Temporal order of events Working memory Damage leads to problems with tasks involving a series of responses ○ Amygdala Memory for emotional significance of experience Strengthens emotionally significant memories in other structures Lesions leads to lack of learned fear ○ Cerebellum and striatum Sensorimotor tasks Cerebellum Stores memories of sensorimotor skills Classical conditioned response Striatum Habit formation (repetitive behavior) Associations between stimuli & responses 2/7/24 1 Emotion, Stress, & Health Emotion: full mind/body/behavior response to a situation 7 primary emotions/expressions - Paul Ekman ○ Sadness Drooping upper eyelids Losing focus in eyes Slightly pulling down of lip corners ○ Happiness Crows feet wrinkles Pushed up cheek Movement from muscle that orbits the eye ○ Fear Eyebrows raised and pushed together Raised upper eyelids Tensed lower eyelids Lips slightly stretched horizontally back to ears ○ Surprise Eyebrows raised Eyes widened Mouth open ○ Anger Eyebrows down and together Eles glare Lips narrow ○ Contempt Lip corner tightened and raised on one side of face ○ Disgust Nose wrinkling Upper lip raised ○ Micro expressions: brief, involuntary facial expressions that reveal a person’s true emotions Guillaume-Benjamin Duchenne ○ Developed techniques to study the muscles and their innervation by using localized electrical stimulation ○ Invented the Duchenne galvanometer (to stimulate specific muscles to map their functions ○ Zygomatic major muscle is critical for producing genuine smiles Duchenne smile Involves the zygomatic major muscle (lifting the corners of the mouth) and the orbicularis oculi muscle (causing the eyes to crinkle) - demonstrating genuine emotion vs voluntary/forced smiles ○ First to provide a detailed clinical description of a specific type of muscular dystrophy in boys (Duchenne muscular dystrophy) Helped distinguish this form of the disease from other neuromuscular disorders ○ One of the first to use photography systematically in medical research Captured images of facial expressions and muscle movements - provided visual aids for understanding his findings and communicating them to others Theories of emotions ○ Common sense view of emotion: suggests that we feel an emotion that leads to a physiological response ○ Cannon-bard theory: emotional stimuli excite both the feeling of emotion in the brain and the expression of emotion in the autonomic and somatic nervous systems - emotional and physiological responses occur simultaneously, mediated by the thalamus ○ James-lange theory: emotions arise as a result of physiological arousal ○ Modern view of emotion: suggests a dynamic interplay between physiological, behavioral, and cognitive components of emotion fMRI scan illustrates areas of increased activity in primary motor cortex and premotor cortex when volunteers watched facial expressions of emotion - same areas were active when the volunteers made the expressions themselves Mirror neurons: neurons that fire both when an individual acts and when they observe the same action performed by others - believed to play a role in empathy and emotional understanding ○ Effects of facial expression on the experience of emotion Participants reported feeling more happy and less angry when they viewed slides while making a happy face, and less happy and more angry when they viewed slides while making an angry face Facial feedback hypothesis: suggests that facial expressions can influence emotional experiences Stress ○ Different definitions “Nonspecific response of the body to any demand made upon it“ (Hans Selye) Physiological reaction caused byperceptionof aversive or threatening situations Increases in sympathetic and HPA activation and as result, increase in glucocorticoid levels H ypothalamic-pituitary-adrenal axis (HPA): key stress response system where the hypothalamus triggers the pituitary gland to release hormones that stimulate the adrenal cortex “Any event in which environmental demands, internal demands, or both tax or exceed the adaptive resources of an individual, social system, or tissue system” (Richard Lazarus) ○ Natural part of life - with appropriate stress management techniques you can learn to manage it more effectively ○ Types Eustress Pleasant, desirable stress - associated w/ exercise or excitement Distress Unpleasant stress i.e. illness or danger Life events can function as stressors Some stressors are chronic Job-related Environmental Hassles Small problems that accumulate to induce major stress Time pressures to get things done Financial concerns Problems in social life In short term, acute stress produces physiological changes that increase the ability to effectively manage the stressor Mobilizes energy, enhances alertness, and temporarily suppresses non-essential functions The center of the mind, body, emotions, and behavior is stress General adaptation syndrome ○ Hans Selye Stressor ○ Brain Anterior pituitary Adrenal cortex Glucocorticoids ○ Hormones that regulate metabolism and immune response during stress Sympathetic nervous system Adrenal medulla ○ Norepinephrine and epinephrine Increased epinephrine Increased heart rate Increased respiration Elevated blood pressure Decreased digestive functions What happens when we are stressed? ○ Good Burst of energy Heightened memory function Burst of increased immunity Lower sensitivity to pain ○ Bad Impaired cognitive performance Suppressed thyroid function Blood sugar imbalance Decreased bone density Higher blood pressure Lowered immunity Increased abdominal fat ○ Order of receiving stressors Hypothalamus Releases Corticotropin-releasing hormone (CRH) Anterior pituitary Releases Adrenocorticotropic hormone (ACTH) (through blood) Adrenal cortex Releases Cortisol Prefrontal regulation during alert, non-stress conditions ○ DMPFC Reality testing Error monitoring DLPFC Top-down guidance of attention and thought rIPFC Inhibition of inappropriate actions VMPFC Regulating emotion A mygdala control during stress conditions ○ → t-cells that attack infected or abnormal ○ Macrophages ingest the microorganism and displays its protein on their cell membranes ○ T cells with an appropriate receptor bind to the macrophage ○ T he bound T cells proliferate and develop into a form that kills body cells that have been infected by the microorganism → b-cells producing antibodies to neutralize pathogens ○ Foreign antigens are bound by B cells with an appropriate receptor Antigen: substance the immune system recognizes as foreign, triggering an immune response ○ The B cells replicate and develop into a form that releases antibodies to the antigen B cells are a class of immune cell that produce antibodies ○ The antibodies bind to the antigens and kill or deactivate the microorganism Immune system cells → t-cells, b-cells, macrophages, and natural killer cells ○ Functions T-cells attack pathogens B-cells produce antibodies Natural killer cells destroy infected cells Macrophages engulf debris and pathogens Cytokine: signaling molecules that mediate and regulate immune responses Gastric ulcers and helicobacter pylori ○ Stress increases susceptibility to ulcers caused by H. pylori bacteria Chronic stress contributes to hypertension and heart disease Bacteria found in mouth and in plaque ○ Streptococcus sanguis ○ Actinobacillus actinomycetemcomitans ○ Porphyromonas gingivalis ○ Tannerella forsythia ○ Treponema denticola S tress effects on the brain: chronic stress can impair hippocampal function, reduces immune efficiency, affect memory, and increase risk for illness Coping with stress ○ Perception and appraisal of stress → individual interpretations of stressors influence levels of stress ○ Perception of control → the belief of control over a stressor reduces its impact ○ Coping strategies Emotion focused coping ○ Involved with trying to reduce negative emotional responses associated with stress instead of addressing the stressor directly ○ May be the only realistic option when the source of stress is outside person’s control Emotion focused strategies ○ Re-appraise situation (challenge - not a threat) ○ Denial or acceptance ○ Keeping yourself busy to take your mind off problem ○ Talking to other people (venting) ○ Ignoring the problem in the hope that it will go away (mental disengagement temporarily) Distracting yourself (i.e. walk, watch TV, games) ○ Building yourself up to expect the worst ○ Praying for guidance and strength ○ Changing how we think about the stressor Problem focused coping ○ Targets the causes of stress in practical ways ○ Planning solutions Seeking social support (asking for help) ○ ○ Problem focused strategies aim to remove or reduce the cause of the stressor Stress reduction techniques ○ Quick ‘time out’ ○ Jacobson’s progressive relaxation ○ Mindfulness/imagery ○ Exercise During periods of stress and strong emotional reactions, the prefrontal cortex loses its regulatory functions
