Physiological Psych notes - Exam 3
Physiological Psych notes - Exam 3 PSYC 3240
Popular in Physiological Psychology
verified elite notetaker
verified elite notetaker
verified elite notetaker
ATM 102- introduction to weather and climate
verified elite notetaker
Popular in Psychlogy
This 10 page Bundle was uploaded by Megan Henry on Sunday January 17, 2016. The Bundle belongs to PSYC 3240 at Clemson University taught by June Plitcher in Summer 2015. Since its upload, it has received 47 views. For similar materials see Physiological Psychology in Psychlogy at Clemson University.
Reviews for Physiological Psych notes - Exam 3
Report this Material
What is Karma?
Karma is the currency of StudySoup.
You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!
Date Created: 01/17/16
Study Soup Sunday, January 17, 2016 10:33 PM SLEEP • College student sleep -‐ 7-‐7.5 weekday, 8 -‐8.5 weekend ○ Major issue is IRREGULARITY § quality not quantity § Timing, duration Ontogeny of sleep • Newborn -‐ polyphasic, 16-‐17 hr/daily ○ 1/2 is REM sleep ○ Premies even more sleep • Children -‐ 9-‐11 • Adolescents -‐ 8-‐10 • Adults -‐ 7-‐8 • Elderly -‐ 5-‐8 ○ Frequent awakenings § Wake up usually once every 90 min cycle § Sometimes can't go back to sleep (very common) ○ SWS deteriorates § Growth hormone released, not needed as much in elderly § As you age, you don't recover from things as quickly □ Protein synthesis slows Endogenous cycles • Circadian rhythms Suprachiasmatic nucleus (SCN) ○ § Controls circadian rhythms § If leisoned, circadian rhythms will no longer exist -‐active/sleep equal parts of the day § Maintains clock through protein synthesis ○ Virtually every process in the body is governed by circadian rhythm • Bunker studies ○ No external light/sun while person is living in the room (college students working on dissertation) ○ 25 hr internal rhythm -‐ no napping, sleep continuously throughout the night; sleeping staggered by an hour each night for a month, then gets erratic ○ Desynchronization: internal rhythms scatter ○ No external light/sun while person is living in the room (college students working on dissertation) ○ 25 hr internal rhythm -‐ no napping, sleep continuously throughout the night; sleeping staggered by an hour each night for a month, then gets erratic ○ Desynchronization: internal rhythms scatter • Light and SNC ○ Nonvisual photoreceptors -‐ tell us if light is present or not § Happening at retinal level § Melanopsin -‐ ganglion cells § Blue light from electronics particularly alerting • Melatonin -‐ prepares you for sleep and seasonal rhythms ○ Produced by pineal gland § Secreted when your body recognizes that it is getting dark outside ○ Hibernation related to melatonin (in other mammals) ○ Naturally decreases with age Sleep motivation • Circadian factor -‐ be awake during the day and asleep at night • Recuperative factor -‐as soon as you wake up, your brain develops the need to sleep again (sleep debt) Shiftwork • Working during the day is best for our health • Evening shifts work well for some-‐ young adults are better suited • Night shifts/work create trouble ○ Can't stop these problems, but we can help them perform better § Working when brain wants to be asleep § Increased sleepiness § Decreased attention and performance § Increased health-‐related problems □ Cardiovascular, gastrointestinal, cancer College life • Studying during the day is best • Avoid studying after about 9 -‐10pm Sleep deprivation • 11 days is the longest • Performance, health, well -‐being • Chronic partial sleep deprivation ○ Catching up on sleep on the weekends HUNGER People who sleep less tend to weigh more • 5 hours of sleep = 3.6% greater BMI • Less sleep, lessl eptin: not hungry hormone • Less sleep, moreg hrelin: hungry hormone Why do we eat too much? HUNGER People who sleep less tend to weigh more • 5 hours of sleep = 3.6% greater BMI • Less sleep, lessl eptin: not hungry hormone • Less sleep, moreg hrelin: hungry hormone Why do we eat too much? • Evolution -‐eat when it was available, our brains don't understand that yet • We store fat in order to "survive", especially women due to estrogen • "What the hell" phenomenon-‐I already ate 3 brownies, what the hell, I might as well eat them all Obesity trends -‐ see link in powerpoint Sympathetic "fight or flight" and Parasympathetic "rest and digest" • PNS allows us to digest food Fuel absorption • Eating -‐ primary fuels of body ○ Carbohydrates (glucose) -‐primary source of energy § Processed food processes through body very quickly into glucose ○ Proteins (amino acids) -‐ lots of energy, bu-termor ○ Fats -‐ mostly storage • Short-‐term reservoir -‐because we are not always eating ○ Liver -‐ glycogen: glucose converts into glycogen (complex glucose), feeds you for ~3h after eating ○ Pancreas -‐ insulin: hormone synthesized and secreted whenever glucose is detected in the blood stream § Allows glucose to be utilized by every muscle cell in the body (fuel) § Takes extra glucose and converts it into glycogen § Unhealthy to have high levels of glucose in the b-‐ high levels of insulin in the blood (diabetes), sugar eats away at your neurons/damages us § Blood sugar levels decrease after eating, insulin stops when there's no more sugar ○ Pancreas -‐ glucagon: fasting hormone, how we access glycogen § Able to break down glycogen -‐ quickly reverted to glucose § Entirely reserved for the bra-‐ brain can ONLY use glucose • Long-‐term reservoir -‐ any glucose that is not immediately being used is stored ○ Triglycerides(fat, adipose tissue) -‐ fat is stored as fat, protein is stored as fat § Glycerol-‐ complex sugar that can be converted to glucose § Fatty acids (stearic acid, oleic acid, palmitic -‐ broken down and used for muscle fuel during fasting § Whenever your pancreas is secreting insulin, your body is storing fat § When insulin is not present, glucagon will burn off this fat • Fasting -‐eating § Glycerol-‐ complex sugar that can be converted to glucose § Fatty acids (stearic acid, oleic acid, palmitic -‐ broken down and used for muscle fuel during fasting § Whenever your pancreas is secreting insulin, your body is storing fat § When insulin is not present, glucagon will burn off this fat • Fasting -‐eating Body weight maintenance • Eating and evolution/adaption -‐ useful for our ancestors, not for us • How to do it: ○ Eat less and be more active ○ Eat wisely (40:30:30) Neural Control of Hunger • Ventromedial hypothalamus (VMH) -‐toward the belly & midline, fat rat syndrome ○ Dynamic stage -‐ first couple of months rats eat a lot and gain weight quickly ○ Static stage -‐eating more food, but not as much as they were in the dynamic stage; weight gain drops off, but still slowly gain weight VMH = center for satiety? -‐ lets you know when your hunger is satisfied ○ § VMH lesion -‐ inc insulin, fat, rat diabetes? • Lateral hypothalamus(LH) -‐ low weight, consistently less food for the rest of their life ○ Nigrostriatal bundle -‐axons § Motor deficits -‐rats didn't want to/had difficulty moving ○ LH = center for hunger-‐ rats wouldn't move but would still eat • Paraventricular nucleus ○ Carbohydrates -‐ food of choice ○ Lesion = fat rat § Different from VMH because VMH eats all foods, PVN focuses on carbs • Brain stem ○ Nucleus of the solitary tract -‐ hunger for carbs ○ Dorsal motor nucleus of the vagu-‐ insulin regulation in response to carbs Chemical Control of Hunger • Fen-‐phen(fenfluramine phentermine) -‐synthetic appetite suppressant ○ 5-‐HT -‐ increases, affective at VMH, LHM, PVN; appetite suppressant ○ Da -‐ increases, feel good ○ Taken off the market because people were having heart attacks, other health risks • Neuropeptide Y (NPY) -‐released within hypothalamus, drastically increases eating • Ghrelin -‐released in stomach, connected to NPY ○ Da -‐ increases, feel good ○ Taken off the market because people were having heart attacks, other health risks • Neuropeptide Y (NPY) -‐released within hypothalamus, drastically increases eating • Ghrelin -‐released in stomach, connected to NPY • Leptin-‐ released from fat tissue, control hunger/feeling of satiety • Cholecystokinin(CCK) -‐released from stomach, feeling full, rats will not eat even if they're hungry REPRODUCTION Neuroendocrine system Glands Exocrine glands- not important in terms of the brain, things like sweat glands (connect directly to target organ) Endocrine glands-‐ connected through blood stream, throughout body Operate through hormones Neruohormones -‐chemically the same as hormone, different in effect on our behavior especially active in the brain, specifically active at the synapse Similar to neurotransmitters, not released in the synapse -‐ broader, longer effect Gonads Testes : sperm-‐ abundantly produced Ovaries : ova (eggs) -‐ set number, gradually released Reproductive activity hormones Androgens : testosterone -‐increases sex drive Estrogens : estradiol-‐ female menstruation Progestins : progesterone -‐ prepares females for gestation Adrenal cortex -‐ near kidneys, releases all 3 hormones ^^ at (lower levels than gonads) Pituitary Gland Tropic hormones-‐ travel through the bloodstream to a specific location Gonadotropic hormones -‐ travel through bloodstream to gonads Follicle-‐stimulating hormones (FSH) Females -‐ stimulates secretion of estrogen, maturation of eggs Males -‐ stimulates sperm production Luteinizing hormone (LSH) Females -‐ stimulates release of ovum during menses cycle (ovulation), release of progesterone Males -‐ stimulates production of testosterone Sex hormones and behavior Gonadectomy Luteinizing hormone (LSH) Females -‐ stimulates release of ovum during menses cycle (ovulation), release of progesterone Males -‐ stimulates production of testosterone Sex hormones and behavior Gonadectomy Males: castration resulted in lowered aggression from less testosterone (Stallions especially); some males decreases aggression, more likely to decrease sexual behavior when done at a young age; when testosterone is reintroduced (by injection) sexual behavior occurs again; some males doesn't have the same effect, especially when done as an adult Females: hysterectomy; without ovaries producing necessary hormones, the female will not mate (except in complex primates) even if estrogen is injected; if testosterone is reintroduced, some sexual behavior will return Pituatary glands Switched male and female pituitary glands -‐males didn't begin to cycle because the hypothalamus is in control Hypothalamus-‐ in control of ALL of our drives, ultimate controller of involuntary sex Medial preoptic area -‐ males: if lesioned, all sexual behavior stops immediately; stimulation results in reproduct-‐ilke behavior; testosterone affinity; twice the size in males than it is in females Ventromedial hypothalamus -‐females: if lesioned, [fat rat syndrome] won't have sex; stimulation results in reproductive -‐like behavior; estrogen affinity; same size in males and females Sexually dimorphic nucleus -‐substantially larger in males than in females; active during sex All ^^ using Da [nucleus accumbens] involved in pleasure Development Systems Bipotential system: fetuses have the potential to become either male or female Wolffian system : embryonic precursor to develop male reproductive ducts (seminal vesicles, vas deferens) Sex determining region -‐ Y chromosome (SRY) Müllerian-‐inhibiting substanc:e stimulates development of WS -‐ testes secrete testosterone & MIS, which causes the MS to degenerate and the testes to descend into the scrotum Genetic females who are injected with testosterone during the fetal period develop male reproductive ducts along with their female ones Androgens Intrauterine -‐ first year to degenerate and the testes to descend into the scrotum Genetic females who are injected with testosterone during the fetal period develop male reproductive ducts along with their female ones Androgens Intrauterine -‐ first year Brain changes -‐ 15% larger than females Müllerian system: embryonic precursor that has the capacity to develop into the female ducts (uterus, fallopian tubes) Occurs in any fetus that is not exposed to testosterone during critical period When things aren't right Turner's Syndrome (XO) Androgen insensitivity syndrome (XY) Look and act like females Genetically male Hyperfeminine Adrenogenital syndrome (XX) High T levels come from adrenal gland Happens after critical perio-‐ can develop extra genitals Internal ovaries External "penis", XL labia Fixed surgically to become female, deactivate T with cortisone High sex drive Homosexuality Little known about Is it a choice? Genetics? Probably a combination of the two Twin studies Identical males -‐ if one was homosexual, 52% chance other would be too Fraternal males -‐ ", 22% Identical females -‐ 48% Fraternal females -‐ 16% Hormones Females -‐ ovulation ~ day 14 Estrogen -‐ good feelings, works with Da & 5-‐HT, makes women want to talk more, be assertive about sex Progesterone -‐less obvious effect, counteracts estrogen, makes women calm/more mellow Testosterone-‐ increases sex drive (peaks during ovulation), assertive, aggressive, seductive Oxytocin -‐ "cuddling" hormone, increases trust levels, more nurturing/helpful, utilizes Da for pleasure from trust, less stress when Progesterone -‐less obvious effect, counteracts estrogen, makes women calm/more mellow Testosterone-‐ increases sex drive (peaks during ovulation), assertive, aggressive, seductive Oxytocin -‐ "cuddling" hormone, increases trust levels, more nurturing/helpful, utilizes Da for pleasure from trust, less stress when talking to opposite sex, released during sex and hugs (in equal amounts), dogs and humans when being pet Vasopressin -‐ water retention, released within kidneys, strong effect in males, females, and most all mammals If you give vasopressin to a male mole rat, he will become monogamous Males Testosterone-‐ makes males more aggressive, dominant, competitive, high sex drive Vasopressin -‐ makes males more attractive in a feminine way (kinder, seems like he wants something long -‐term, as opposed to T just for sex), gallantry, monogamy, increases after a baby is born, increases ability for males to hear a baby cry Oxytocin -‐ same as in females Prolactin -‐ stimulates males to make connections, increases after baby is born, attachment, decreases sex drive Estrogen -‐ little effect on males, bthe-‐scenes, it seems to drive other hormones and make them more manly/powerful Female/Male interaction Females Power of estrogen -‐ communication and cooperation Stress -‐ communicate (can't run), evolutionay ren't able to flee with a child Males Androgens -‐competition and sex Stress -‐ fight or flight Females feel distressed when they are forced to fight Hypothalamus, hippocampus (working memory doesn't work well during stress in females), amygdala (overreaction) Environmental influences Multiple births (litters) -‐ if a male is born into an all female litter he will have more estrogen, and likewise Pheromones: scents given off Females cycle together T-‐shirt studies -‐ males more attracted to female scent when they are ovulating, unless it is their sister Reproduction choices -‐ overpopulation? Pheromones: scents given off Females cycle together T-‐shirt studies -‐ males more attracted to female scent when they are ovulating, unless it is their sister Reproduction choices -‐ overpopulation? MY PSYCH LAB BRAIN DAMAGE AND NEUROPLASTICITY Hippocampus-‐ spatial location and neurogenesis Olfactory bulb -‐ output goes to amygdala, platform cortex; neurogenesis Neuron degeneration -‐axon separates from cell body ("soma"), caused by trauma or diseases Anterograde degeneration -‐ axon degenerates b/w cut and terminal endings, postsynaptic neurons lose input Retrograde degeneration -‐axon degeneration of proximal segment (up to soma-) leads to death and loss of neurons Chromatolysis -‐ breakdown process involving increased protein synthesis after neuron death, glial cells clean up Transneuronal degeneration -‐ once the axon is dead, surrounding neurons begin to die Damage -‐ neurons may respond with excessive depolarization from loss of oxygen or glucose Stroke-‐related ischemia: loss of blood flow due to blockage Shown to happen in neurons that release glutamate. Normal reuptake processes fail, therefore postsynaptic targets are flooded with glutamate Influx of calcium and zinc ions -‐ triggers self destruct (excitotoxicity) Secondary excitotoxicity can lead to further damage in the body Apoptosis: programmed cell death, safer than necrosis -‐ don't release anything (like NT) into extracellular fluid Can lead to secondary damage in brain Recovery techniques: collateral sprouting, dendritic branching, neurogenesis, cortical reorganization Collateral sprouting : axons grow out of existing healthy axons to replace those that are lost (like a bypass surgery) Dendritic branching : dendritic arboration -‐grows out of dendrite in a tree-‐like fashion (rooted, grows up and out, branches) Improved motor function in rats post -‐stroke Stem cells: undifferentiated cells, can be influenced into functioning wherever they are put in the brain Cortical reorganization -‐ after brain damage, healthy neurons are assigned to pick up the sensory information from the damaged area "phantom limb syndrome" they are put in the brain Cortical reorganization -‐ after brain damage, healthy neurons are assigned to pick up the sensory information from the damaged area "phantom limb syndrome"
Are you sure you want to buy this material for
You're already Subscribed!
Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'