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Physiological Psych notes - Exam 3

by: Megan Henry

Physiological Psych notes - Exam 3 PSYC 3240

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Megan Henry

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About this Document

These notes cover the topics of: sleep, hunger, reproduction, and MyPsychLab.
Physiological Psychology
June Plitcher
Psychology, physiological psychology, neuropsychology
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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.


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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"


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