Exam 5

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Exam 5
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2011-07-12 16:04:37
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  1. aMSH and CART location
    Arcuate nucleus is the locatio of what anorexic peptides?
  2. TSH and ACTH are inhibited by what peptides?
    NPY and AgRP inhibits the secretion of what?
  3. What peptides are Anorectic (stop eating)?
    aMSH and CART inspire what kind of eating behavior?
  4. What peptides are Orexigenic (stimulate eating)?
    NPY and AgRP stimulate what kind of behavior?
  5. Which peptides are antagonistic to eachother?
    AgRP and aMSH both bind to the MC4 receptor therefore they are ____________to eachother.
  6. Which four peptides stimulate eating behavior?
    NPY, AgRP, MCH, and Orexin all do what?
  7. MCH and Orexin are located where?
    Which two peptides come from the Lateral hypothalamic area?
  8. What axons contribute to feeding behavior?
    Axons both with bodys in the lateral hypothalamus, and just passing through contribute to what behavior?
  9. What involvement does the Cortex have in regulating behavior?
    Which part of the brain is invovled in organizing and initiating goal-directed behaviors?
  10. Which system informs the cortex of Leptin levels?
    The MCH system informs the cortex of what?
  11. What happens when MCH is injected in the brain?
    Feeding behavior is stimulated when what peptide is injected into the brain?
  12. What happens to Leptin levels when body fat is increased?
    Leptin levels increase when fat levels _______
  13. A rise in Leptin levels causes what?
    aMSH and CART are released in the arcuate nucleus causing feeding behavior to be inhibited and metabolism to increase.
  14. A fall in Leptin levels increases what kind of peptides in the arcuate nucleus and lateral hypothalamic area?
    A ____ in leptin levels causes the release ofe NPY and AgRP and MCH.
  15. Orexigenic peptides cause what kind of feeding behavior and what effect on metabolism?
    What kind of peptides act on the brain to stimulate feeding behavior and decrease metabolism?
  16. What are the three phases of shor-term regulation of feeding behavior?
    • 1. Cephalic phase
    • 2. Gastric phase
    • 3. Substrate phase
  17. What happens in the cephalic phase?
    sight and smell of food trigger parasympathetic and eteric divisions of ANS (drooling over pancakes and digestive stomach juices are flowing)
  18. What happens in the Gastric Phase
    more saliva, more stomach juices as you chew and swallow food
  19. Substrate phase
    stomach starts to fill and the food (chyme) passes into intestines where nutrients are absorbed.
  20. Ghrelin (my stomach is ghrelin!) activates the release of what?
    NPY and AgRP is activated by what peptide in the stomach?
  21. Why does the meal have to end?
    the action of the three satiety signals: gastric distention, release of cholecystokinin (CCK), and release of insulin cause what?
  22. How do the axons from the stomach get to the brain?
    The vagus nerve is the route by which axons from where go to the brain?
  23. What neurons do the vegas nerve axons stimulate to inhibit feeding behavior?
    The neurons in the nucleus of the solitary tract in the medulla are stimulated by what nerve? (the wanderer stimulates the solitary)
  24. CCK is found where and what does it do?
    This peptide is found in cells lining the intestines (a little is in the CNS too) and is activated by certain foods (esp. fat) and works with distention to inhibit feeding behavior.
  25. Insulin is required to transport what where?
    what is required to transport glucose into cells other than neurons?
  26. How does blood born insulin effect the arcuate and ventromedial nuclei of the hypothalamus?
    Which peptide acts about the same as Leptin on the arcuate and ventromedial nuclei?
  27. What does hedonic mean?
    It feels good so you do it
  28. Drive reduction refers to what?
    the act of satisifying a craving
  29. Where are the most effective sites for self-stimulation?
    along the trajectory of dopaminergic axons arising in the ventral tegmental area and projecting to the forebrain.
  30. What does dopamine released in the brain do?
    Behavior is reinforced by the release of what in the brain?
  31. Dopamine depletion effects food behavior how?
    the animal will act as if it likes food but does not want food when what is depleted?
  32. What happens to seratonin levels in the hypothalamus during the three periods of eating?
    Low in post absorptive, rising in anticipation, and spike durring a meal.
  33. What amino acid is seratonin derived from?
    Tryptophan is used to derive what?
  34. What effects the amount of tryptophan in the blood?
    Chocolate chip cookies! Aka carbs
  35. Irregularities in brain seretonin may effect what kind of disorders?
    Eating!
  36. In which eating disorder is seratonin most strongly linked?
    Bulemia nervousa is often treated with Prozac because it is linked with regulation of what?
  37. Hypovolemia is a decrease in what?
    What is a decrease in blood volume called?
  38. What is hypertonicity?
    An increase in the concentration of dissolved substances in the blood is called what?
  39. Volumetric thirst is caused by what?
    Hypovolemia triggers what kind of thirst?
  40. How is hypovolemia detected?
    first angiotensin II is released activating neurons in the subfornical organ of the kidney, then mechanosensory axons in the vagus nerve activate neurons in the nucleus of the solitary tract these send signals to the hypothalamus.
  41. Where is hypertonicity of the blood sensed?
    The vascular organ of the lamina terminalis (OVLT) loses water and this causes a change in the actions potential firing frequency.
  42. What do the OVLT neurons do?
    • 1. directly excite the magnocellular neurosecretory cells that secrete vasopressin.
    • 2. stimulate osmometric thirst
  43. What is the motivation to drink water when dehydrated called?
    Osometric thirst motivates you to do what?
  44. Lesions of OVLT prevent responses to dehydration but not what?
    Responses to loss of blood volume are not effected by lesions of what hypothalamic area?
  45. What causes diabetes insipidus and what are it's effects?
    Selective loss of the vasopressin-secreting neurons of the hypothalamus and the body working against the brain is called what?
  46. How is diabetes insipidus treated?
    Replacing lost vasopressin treats what disease?
  47. Where are the important neurons for temperature homeostasis located?
    clustered in the anterior haypothalamus are neurons improtant for what?
  48. Where are humoral and visceromotor responses to temperature change intitiated?
    The medial preoptic area of the hypothalamus initiates what kind of responses to a change in temperature?
  49. Somatic motor (behavior) responses to temp. change happen where?
    The lateral hypothalamic area initiates what kind of response to temp changes?
  50. sex-determining region of the Y chromosome (SRY) codes for a protien called what?
    testis-determining factor
  51. androgens are found more in
    Males have more of these
  52. estrogens are found more in which sex?
    Women have more of these hormones
  53. What is estradiol synthesized from?
    with the aid of aromatase testoterone is converted into what?
  54. What are the principal female hormones?
    estrodial and progesterone are the principle hormones for which sex?
  55. which parts of the brain control sex hormones?
    the pituitary gland and the hypothalamus control what kind of hormones?
  56. The anterior pituitary gland secretes what two hormones?
    Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) aka gonadotropins are released where?
  57. What hormone released from the hypothalamus causes the release of LH and FSH?
    Gonadotropin-releasing hormone (GnRH) aka lutenizing hormone-releasing hormone (LHRH) cause what to be released from where?
  58. Light inhibits melatonin production on what gland?
    the pineal gland
  59. More light means less meletonin which means more what?
    gonadotropin
  60. What does an injection of vasopressin in a male vole do?
    The male will form an intense bond with the female vole even without mating
  61. Oxytocin does what for females?
    It stimulates pair bonding, smooth muscle (contractions), and lactose let down reflex (breastfeeding).
  62. What is the estrous cycle?
    It is characterised by a shorter luteal phase.
  63. What is the luteal phase?
    this is after egg expulsion when the cells surrounding the egg undergo chemical changes (depends on LH reliese in the pituitary)
  64. What are engorgement and erection controled by?
    axons in the parasympathetic division of ANS in spinal cord (from thoughts in the brain) or mechanical stimulation
  65. What do the parasympathetic nerve endings release durring erection and engorgement?
    ACh, vasoactive intestinal poypeptide (VIP), and nitric oxide (NO).
  66. What must be activated to complete the sexual response?
    In the sympathetic division of the ANS sensory axons become highly active. Ejaculation occurs, then resolution.
  67. What does vasopresin (aka ADH) do besides pairbond men to women?
    helps regulate water and salt levels in the body (mainly by affecting the kidneys)
  68. sexual dimorphisms
    the differences in male and female brains
  69. There is a large difference in the human male and female brain.
    False
  70. Where is the sexually dimorphic nucleus (SDN) located?
    In the preoptic area of the anterior hypothalamus
  71. The SDN is five to eight times larger in females than in males
    False
  72. Give an example of neurotransmitters that may be involved in controlling monogamy vs polygamy
    Vasopressin may contribute to male monogamy and Oxytocin may contribute to female monogamy.
  73. Describe a few of the regions of the brain where sexual dimorphisms are most evident
  74. Describe the sexual dimorphisms in cognition
  75. Distinguish between organizational and
    activational effects of sex steroids on the brain and its function.
  76. Give examples of and describe mismatches of genetic sex and hormone action for androgen insensitivity
  77. Give examples of and describe mismatches of genetic sex and hormone action for congenital adrenal hyperplasia
  78. describe the some of the activational effects that sex steroids have on the brain
  79. List some of the brain areas that may be involved in sexual orientation
  80. Compare and contrast the James-Lange Theory and the Cannon-Bard Theory of emotion
    • James-Lange said that emotion is a response to physiological changes.
    • Cannon-Bard said that emotional experience can occur independently of emotional expression.
  81. What is an unconscious emotion?
    expression of emotion without conscious awareness of the stimulus that evoked the emotion.
  82. Briefly describe the historical contribution of
    Paul Broca to our understanding of the limbic system.
    Found the limbic lobe, looked like a border (limbic is latin for border). First thought to be for olfaction, later with emotion.
  83. Describe the anatomy, connectivity and function
    of each region associated with the Papez
    circuit.
    Neocortex (emotional coloring or volume) --> Cingulate cortex (emotional experience) --> Hippocampus --> fornix --> Hypothalamus (emotional expression) --> Anterior nuclei of thalamus --> Cingulate cortex etc.
  84. Describe Kluver-Bucy Syndrome and list the
    effects of bilateral temporal lobectomy.
    • temporal lobectomy: bilateral removal of temporal lobes
    • good visual perception but poor recognition
    • oral tendencies
    • hypersexuality
    • "flattened" emotions
  85. Describe the cytoarchitecture of the amygdala, be able to label its connections (both incoming and outgoing)
    Three parts 1. basolateral nuclei (visual, auditory, gustatory, and tactile afferents) 2. corticomedial nuclei (olfactory afferents) 3. central nucleus
  86. What is the effect of removing the amygdala on
    the behavior of an animal?
    • they become docile, decreases agression.
    • inability to percieve fear and anger
  87. Describe the effect of electrically stimulating the amygdala
    • medial hypothalamus: affective agression
    • lateral hypothalamus: preditory agression
  88. Describe the circuitry for learned fear.
  89. Distinguish between predatory and affective aggression
    • predatory: obtaining food (not sympathetic)
    • affective: a show of strength
  90. Describe the role of the hypothalamus in aggression.
    posterior hypothalamus is important in expression of anger and aggression and normaly inhibited by the telencephalon.
  91. Describe the role of the midbrain in aggression
    • two major pathways
    • medial forbrain bundle --> ventral tegmental (preditory aggression when stimulated)
  92. Describe the effect of Serotonin on aggressive behavior. (Be able to discuss the effect of seratonin knock out mice and the use of agonists and antagonists to the 5-HT receptor.)
    • drugs that block synthesis or release of serotonin increases aggression (aggressive monkeys lose their status)
    • agonist decreases aggression
    • antagonists increase aggression
  93. Describe the contributions of Richard Canton and
    Hans Berger in the development of the EEG.
    made electrical recordings from surface of dog and rabit brains.
  94. Describe how an EEG is performed and what is
    being recorded.
    • electrodes taped to the scalp with conductive paste
    • the record is a set of many simultaneous squigles indicating voltage changes between pairs of electrodes
  95. Describe the basic forms of EEG rhythms and what they indicate
    • Beta rhythms: fastest 14 and up Hzm- high consentration
    • Alpha rhythms: 8-13 Hz - awake and calm
    • Theta rhythms: 4-7 Hz - REM?
    • Delta rhythms: less than 4 Hz.-deep sleep
  96. Describe the concepts of how synchronous rhythms are generated in the brain
    • 1. all take cues from pacemaker/central clock (conductor)
    • 2. share the timing function: mutually exciting or inhibiting eachother (jam session)
  97. What are the functions of brain rhythms?
    • 1. rhythms block info
    • 2. synchrony binds so you have one perceptual experience
    • 3. no direct function, just an interesting by-product
  98. Compare and contrast generalized seizures and partial seizures.
    • generalized: all over the brain
    • Partial: parts of the brain
    • both types fire with synchrony that never occurs during normal behavior.
  99. Define epilepsy and define the classes of drugs that may act as convulsants and anticonvulsants.
    • GABA blocker promotes seizures (convulsants)
    • GABA agonists (anticonvulsants) like barbituates and benzodiazepines.
  100. Define the following terms are related to seizures: tonic, clonic, aura, deja vu
    • tonic: ongoing
    • clonic: rythmic
    • aura: abnormal sensory sensation
    • deja vu: well formed auras
  101. Why are observing the onset of partial seizures important?
    sometotopic mapping
  102. Define sleep and compare and contrast its three functional states
    redily reversible state of reduced responsiveness to, and interaction with, the environment.
  103. Describe the stages of the sleep cycle
    • 1. non-REM an idling brain in a moveable body
    • 2. sleep spindle: slightly deeper 5-15 minutes
    • 3. EG large amplitude slow delta rythms (little movement)
    • 4. Deepest large EEG rythms 20-40 minutes

    2. REM dreaming sleep, and active brain in an immobile body.
  104. Describe the features of somnambulism
    sleep walking
  105. Describe the general theories regarding the function of sleep.
    • restoration: fixes your body while you sleep
    • adaptation: protects you from night dangers
  106. Location of the SRY gene
    the short (p) arm of the Y chromosome
  107. TDF (testese determining factor) is coded by what gene?
    SRY gene a small segment near the tip of the short arm of the Y chromosome codes for what?
  108. Efferents from the central nucleus
    • hypothalamus --> autonomic response
    • Periaqueductal gray matter in brain stem --> behavioral reaction
  109. Efferent from basolateral nuclei (auditory)
    Cerebral cortex --> emotional experience
  110. Neural circuit for aggression
    Cerebral cortex --> amygdala ==> Hypothalamus & PAG --> aggressive behavior
  111. Describe the functions of Dreaming and REM
    sleep. (Include the finding of Hobson-McCarley and Avi Karni).
    • Hobs- said freud was an idiot and sleep is to improve memory
    • Avi- learning/sleep study they improved.
  112. Describe the neural principle of the mechanisms
    of sleep
    see page 602
  113. Discuss the functions of the reticular activating system (Giuseppe Moruzzi)
  114. Describe the process of falling asleep and list
    the neurotransmitters involved in the process.
  115. Describe the activity patterns in the brain
    associated with the stages REM and Non-REM sleep and wake cycles.
  116. Define circadian rhythms and how they are
    controlled by zeitgebers
  117. Describe the centers of the brain that are important in forming the biological clock.
  118. Describe the mechanism by which light and dark cycles send input to the hypothalamus
  119. List the genes and cellular mechanisms within the SCN
    that control timing in the brain and body. (Who discovered the CLOCK gene?)
  120. Components of Broca's aphasia
    • non-fluent
    • lack gramatical words
    • problem with verb conjugation
    • paraphasic (incorect sound for a word)
    • anomia (difficulty finding and producing words)
  121. Components of Wernicke's aphazion
    • meaningless speach
    • more paraphasic errors
    • don't understand most requests
  122. Is Wernicke's area a speach/sound control area?
    Not exactly because Broca's area works just fine without it.
  123. Wernike-gershwin model of repeating a spoken word
    primary auditory cortex--> wern's area --> arcuate fasciculus --> broca --> motor cortex
  124. What happensin Werneke's area?
    Processes the sound and produces the meaning
  125. What happens in the arcuate fasciculus?
    word signals from werneke's area are converted and sent to Broca
  126. What happens in Broca's area?
    word signals are converted to code for muscle movements required for speach. These signals are sent to the motor cortex

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