Bio Psychology Exam 3 Answers
Content
Biopsychology Exam 3 Answers 1. A hormone is a chemical that is secreted by a gland or other cells and is transported by blood vessels to other organs where it alters activity. Hormones are secreted by the endocrine gland and result in long lasting changes in the body. 2. The anterior pituitary gland acts like glandular tissues and releases different hormones while the posterior pituitary gland acts like neuronal tissue and is physically connected to the hypothalamus through blood vessels. 3. Anterolateral pathway 4. Central temperature receptors are in the preoptic area and anterior hypothalamus and have warm and cold sensitive neurons. 5. In response to heat, the medial preoptic area decreases the production of TSH which increases parasympathetic activity and results in the dilation of cutaneous vessels, and acceleration of respiration and perspiration. 6. In response to cold, the medial preoptic area increases the production of TSH and increases sympathetic activity resulting in the constriction of cutaneous vessels, metabolism of brown fat, and shivering of muscles. 7. Osmotic thirst results from eating too many salty foods. Hypovolemic thirst results from losing fluid through blood or sweat. 8. Receptors for osmotic thirst are in the stomach and duodenum and OVLT. 9. Receptors for hypovolemic thirst are in the heart and kidney. 10. For the heart, the information travels through the vagus nerve, and for the kidney, the information travels through production of renin. 11. The kidneys release renin which helps form angiotensin II which stimulates the preoptic area and causes vasopressin release and water conservation. 12. In the absorptive phase, food is actively being taken in and insulin level is high so cells can metabolize glucose and convert extra glucose into glycogen where it is stored in the muscles and liver. 13. In the fasting phase, when you’re not actively taking energy the sympathetic system increases, glucagon takes glycogen and turns it glucose, and insulin level decreases. 14. Basal metabolism is when you are doing nothing, or vegetative state. 15. The brain can only use glucose but doesn’t need insulin for the cells to metabolize it. 16. Short term storage occurs in the liver and muscles as glucose and glycogen, and long term storage occurs in the adipose tissue as fat. 17. When you have low blood glucose, the pancreas releases glucagon which converts the glycogen in the liver and muscles to glucose and releases it in the blood stream. 18. If you have high blood glucose level, the pancreas secretes insulin which allows cells to increase consumption of glucose or the storage of extra glucose. Beta cells release insulin. 19. In Type I diabetes, the autoimmune system destroys beta cells which results in net loss of insulin production.
20. In type II diabetes, insulin doesn’t work properly or the body cells don’t respond to insulin which prevents cells from taking insulin in and results in high blood glucose. 21. Set point theory states that there is a range of feeling comfortablehungryeating as energy goes down and goes up. 22. A combination of social/environmental factors (eating 3 times a day), dietary selection, and physiological hunger signals. 23. Learned eating in response to an external cue. 24. Sensory specific satiety is satiety for one type of food in the absence of general satiety. It allows people to eat varied amounts and more food. 25. Glucoprivation and lipoprivation are the physiological hunger signals that stimulate eating and they are detected in the nucleus of solitary tract (NST) detects glucoprivation and the liver detects both. 26. Gastrointestinal factors (CCK) and long term satiety. 27. CCK is a satiety peptide hormone that is secreted from the gut (duodenum) and since it doesn’t cross the blood brain barrier, it sends a satiety signal through the vagus nerve. 28. Fat cells secrete leptin which reaches arcuate nucleus of hypothalamus and inhibits neuropeptide y (hunger peptide) and promotes melanocortins (satiety peptides). Leptin receptor activation also increases corticotrophin releasing hormone which suppresses hunger. 29. A mutation in the ob gene causes cells to be unable to produce leptin so there is nothing suppressing hunger. 30. The NST/AP receives sensory information from the internal organs through the vagus nerve. 31. Lesioned NST results in loss of glucoprivation and lipoprivation induced feeding. 32. The lateral hypothalamus is the hunger center, a lesion to it results in aphagia. The Ventromedial hypothalamus (VMH) is the satiety center and a lesion to it results in hyperphagia (excessive eating). 33. A lesion to the VMH results in increased parasympathetic system and high insulin levels and low glucagon levels, animals store the glucose as glycogen but cannot turn the glycogen back in to glucose. This results in constant hunger. 34. 2nd messenger systems 35. Hormones derived from cholesterol that contain 4 carbon rings 36. Steroid hormones can act in 3 ways: binding to membrane receptors, entering cells and activating proteins in cytoplasm, entering nucleus and binding to chromosomes which influences gene activation. 37. Stress (cortisol/ corticosterone) and sex hormones 38. Stress hormones are released by the adrenal glands and induce breakdown of fats and protein to provide energy. 39. Gonads 40. Chromosomal sex genetic sex hormonal sexmorphological sexbehavioral sex
41. Father’s sperm. Default is XX. 42. The SRY is a region on the Y chromosome that releases testes determining factor (TDF) which causes the formation of the testes which produce testosterone. 43. Testes make testosterone and AMH (anti mullerian hormone). 44. Testosterone promotes the development of the wolfian system (male reproductive system) and AMH inhibits development of mullerian system (female reproductive system). 45. 4-6 weeks after fertilization 46. The urogenital sinus differentiates into male or female genetalia. 47. DHT is needed for development of male external genetalia. It is converted from testosterone to DHT by 5-alpha reductase. 48. If there are no androgens, the default female setting is developing female genetalia. 49. Genetic XY males are insensitive to androgens and they make testosterone and AMH but cannot respond. Internal genitals are male but external genitals look like female. 50. Testosterone cannot be converted to DHT and external male genitals cannot form. 51. The adrenal glands product too much androgens instead of cortisol and high levels of Testosterone and DHT result in male external genitals. 52. Testosterone can bind to receptors in the brain and influence at the DNA level and make a male brain. 53. The preoptic area is sexually dimorphic in size and is bigger in males than females. 54. According to the aromatization hypothesis, testosterone is converted into estrogen by the aromatase enzyme and this estrogen blocks apoptosis for males. For females, the estrogen is soaked upby the alpha-fetoprotein and cannot act on the brain. 55. During the preovulatory period, the surge of estrogen and progesterone make females more receptive to sexual stimuli and more selective towards a mate who looks masculine. 56. Lordosis is a sexual behavior where the female positions herself to receive the male and this occurs because of high estrogen and progesterone levels. 57. The ventromedial nucleus is important for display of female sexual behavior. When estrogen level of VMH is absent, females show no sexual receptive behavior and reject more. 58. Male sexual behavior declines in the absence of testosterone and if lesions to the mPOA are made. 59. Dopamine agonist increases dopamine activity in mPOA and results in more ejaculations. 60. Regulates female maternal behavior 61. Released before you go into labor, stimulates milk production, and is also released during an orgasm which promotes pair bonding and mother child interaction. 62. The interstitial nucleus of anterior hypothalamus (INAH) is larger in He-M than Ho-M and He-F. The anterior commissure is larger in He-F and Ho-M than He-M. He-F an HoM brains are activated by pheromones but not He-M. 63. Males have bigger brains but females have more folds
64. Boys draw mobile and mechanical objects with dark colors and from a birds eye view. Girls draw human motifs and flowers and butterflies with warm colors arranged in a row on the ground. 65. Women are more sensitive to musk like odors under the influence of hormones. Women are better at discriminating tastes. Women have louder EOAEs than men from birth. Men have better visual acuity but women have higher tolerance for light intensity. 66. Stage 1Stage 2 Stage 3 Stage 4Stage 3 Stage 2REMStage2, 3,4,3,2awake. 67. Each sleep cycle is 90-110 minutes long. 68. During waking state, there are two EEG patterns depending on whether you are relaxed or attentive. When you are relaxed, there are alpha waves which have low frequency, high amplitude and are synchronous. When you are attentive, beta activity shows high frequency, low amplitude and asynchronous. 69. Awake-alpha & beta activity. Stage 1- Theta activity. Stage 2- Sleep spindles and K complex. Stage 3- Delta. Stage 4- Delta. REM- Theta and Beta activity. 70. Stage 1 sleep, REM sleep, when animals are doing behaviors related to species survival. 71. Dreaming occurs doing REM sleep. Also, there is inhibition of motor neurons so your body is paralyzed. 72. Brain stem neurons 73. In REM sleep, there is EEG desynchrony, lack of muscle tone, clitoral or penile errection and irregular heart rate and perspiration. In NREM sleep, thee is EEG synchrony, moderate muscle tone, absence or slow eye movements, lack of genital activity and decreased heart rate and respiration. 74. During REM sleep, different parts of the reticular formation come active and each controls different aspects of REM sleep. 75. The basal forebrain makes Acetylcholine (Ach) and lesions to it cause insomnia. 76. mPOAH inhibits Acetylcholine and cortex and basal forebrain area cannot be in the active or alert state. 77. The raphae nuclei produces serotonin which causes cortical arousal. Lesions cause insominia. 78. Increase in GABA causes sleep (Benzodiazepine). Increase in adenosine causes sleep. Increase in Histamine causes arousal. 79. Melatonin is made in the pineal gland and dim light increases melatonin which increases sleep. 80. What is the evolutionary theory of sleep? 81. What is recuperation theory and what are evidences for it? 82. What is circadian theory? 83. What is the circadian rhythm? 84. What are zeitgebers? 85. Where is the biological clock in the brain and what is its function?
86. What happens if there is a lesion to the SCN, stimulation, transplant? 87. Where is the body’s molecular clock and how does it work? 88. What is the activation synthesis theory? 89. What is reverse learning theory? 90. What is memory consolidation theory and evidence for it? 91. What are the correlations between REM sleep and learning? 92. What is the correlation between REM sleep and behavioral performances? 93. What is the correlation between REM sleep deprivation and memory? 94. What types of learning are not affected by REM sleep deprivation? 95. What is insomnia? 96. What is sleep apnea? 97. What are periodic limb disorder movements? 98. What is narcolepsy? 99. What is REM sleep without atonia? 100. What role does orexin play?
20. In type II diabetes, insulin doesn’t work properly or the body cells don’t respond to insulin which prevents cells from taking insulin in and results in high blood glucose. 21. Set point theory states that there is a range of feeling comfortablehungryeating as energy goes down and goes up. 22. A combination of social/environmental factors (eating 3 times a day), dietary selection, and physiological hunger signals. 23. Learned eating in response to an external cue. 24. Sensory specific satiety is satiety for one type of food in the absence of general satiety. It allows people to eat varied amounts and more food. 25. Glucoprivation and lipoprivation are the physiological hunger signals that stimulate eating and they are detected in the nucleus of solitary tract (NST) detects glucoprivation and the liver detects both. 26. Gastrointestinal factors (CCK) and long term satiety. 27. CCK is a satiety peptide hormone that is secreted from the gut (duodenum) and since it doesn’t cross the blood brain barrier, it sends a satiety signal through the vagus nerve. 28. Fat cells secrete leptin which reaches arcuate nucleus of hypothalamus and inhibits neuropeptide y (hunger peptide) and promotes melanocortins (satiety peptides). Leptin receptor activation also increases corticotrophin releasing hormone which suppresses hunger. 29. A mutation in the ob gene causes cells to be unable to produce leptin so there is nothing suppressing hunger. 30. The NST/AP receives sensory information from the internal organs through the vagus nerve. 31. Lesioned NST results in loss of glucoprivation and lipoprivation induced feeding. 32. The lateral hypothalamus is the hunger center, a lesion to it results in aphagia. The Ventromedial hypothalamus (VMH) is the satiety center and a lesion to it results in hyperphagia (excessive eating). 33. A lesion to the VMH results in increased parasympathetic system and high insulin levels and low glucagon levels, animals store the glucose as glycogen but cannot turn the glycogen back in to glucose. This results in constant hunger. 34. 2nd messenger systems 35. Hormones derived from cholesterol that contain 4 carbon rings 36. Steroid hormones can act in 3 ways: binding to membrane receptors, entering cells and activating proteins in cytoplasm, entering nucleus and binding to chromosomes which influences gene activation. 37. Stress (cortisol/ corticosterone) and sex hormones 38. Stress hormones are released by the adrenal glands and induce breakdown of fats and protein to provide energy. 39. Gonads 40. Chromosomal sex genetic sex hormonal sexmorphological sexbehavioral sex
41. Father’s sperm. Default is XX. 42. The SRY is a region on the Y chromosome that releases testes determining factor (TDF) which causes the formation of the testes which produce testosterone. 43. Testes make testosterone and AMH (anti mullerian hormone). 44. Testosterone promotes the development of the wolfian system (male reproductive system) and AMH inhibits development of mullerian system (female reproductive system). 45. 4-6 weeks after fertilization 46. The urogenital sinus differentiates into male or female genetalia. 47. DHT is needed for development of male external genetalia. It is converted from testosterone to DHT by 5-alpha reductase. 48. If there are no androgens, the default female setting is developing female genetalia. 49. Genetic XY males are insensitive to androgens and they make testosterone and AMH but cannot respond. Internal genitals are male but external genitals look like female. 50. Testosterone cannot be converted to DHT and external male genitals cannot form. 51. The adrenal glands product too much androgens instead of cortisol and high levels of Testosterone and DHT result in male external genitals. 52. Testosterone can bind to receptors in the brain and influence at the DNA level and make a male brain. 53. The preoptic area is sexually dimorphic in size and is bigger in males than females. 54. According to the aromatization hypothesis, testosterone is converted into estrogen by the aromatase enzyme and this estrogen blocks apoptosis for males. For females, the estrogen is soaked upby the alpha-fetoprotein and cannot act on the brain. 55. During the preovulatory period, the surge of estrogen and progesterone make females more receptive to sexual stimuli and more selective towards a mate who looks masculine. 56. Lordosis is a sexual behavior where the female positions herself to receive the male and this occurs because of high estrogen and progesterone levels. 57. The ventromedial nucleus is important for display of female sexual behavior. When estrogen level of VMH is absent, females show no sexual receptive behavior and reject more. 58. Male sexual behavior declines in the absence of testosterone and if lesions to the mPOA are made. 59. Dopamine agonist increases dopamine activity in mPOA and results in more ejaculations. 60. Regulates female maternal behavior 61. Released before you go into labor, stimulates milk production, and is also released during an orgasm which promotes pair bonding and mother child interaction. 62. The interstitial nucleus of anterior hypothalamus (INAH) is larger in He-M than Ho-M and He-F. The anterior commissure is larger in He-F and Ho-M than He-M. He-F an HoM brains are activated by pheromones but not He-M. 63. Males have bigger brains but females have more folds
64. Boys draw mobile and mechanical objects with dark colors and from a birds eye view. Girls draw human motifs and flowers and butterflies with warm colors arranged in a row on the ground. 65. Women are more sensitive to musk like odors under the influence of hormones. Women are better at discriminating tastes. Women have louder EOAEs than men from birth. Men have better visual acuity but women have higher tolerance for light intensity. 66. Stage 1Stage 2 Stage 3 Stage 4Stage 3 Stage 2REMStage2, 3,4,3,2awake. 67. Each sleep cycle is 90-110 minutes long. 68. During waking state, there are two EEG patterns depending on whether you are relaxed or attentive. When you are relaxed, there are alpha waves which have low frequency, high amplitude and are synchronous. When you are attentive, beta activity shows high frequency, low amplitude and asynchronous. 69. Awake-alpha & beta activity. Stage 1- Theta activity. Stage 2- Sleep spindles and K complex. Stage 3- Delta. Stage 4- Delta. REM- Theta and Beta activity. 70. Stage 1 sleep, REM sleep, when animals are doing behaviors related to species survival. 71. Dreaming occurs doing REM sleep. Also, there is inhibition of motor neurons so your body is paralyzed. 72. Brain stem neurons 73. In REM sleep, there is EEG desynchrony, lack of muscle tone, clitoral or penile errection and irregular heart rate and perspiration. In NREM sleep, thee is EEG synchrony, moderate muscle tone, absence or slow eye movements, lack of genital activity and decreased heart rate and respiration. 74. During REM sleep, different parts of the reticular formation come active and each controls different aspects of REM sleep. 75. The basal forebrain makes Acetylcholine (Ach) and lesions to it cause insomnia. 76. mPOAH inhibits Acetylcholine and cortex and basal forebrain area cannot be in the active or alert state. 77. The raphae nuclei produces serotonin which causes cortical arousal. Lesions cause insominia. 78. Increase in GABA causes sleep (Benzodiazepine). Increase in adenosine causes sleep. Increase in Histamine causes arousal. 79. Melatonin is made in the pineal gland and dim light increases melatonin which increases sleep. 80. What is the evolutionary theory of sleep? 81. What is recuperation theory and what are evidences for it? 82. What is circadian theory? 83. What is the circadian rhythm? 84. What are zeitgebers? 85. Where is the biological clock in the brain and what is its function?
86. What happens if there is a lesion to the SCN, stimulation, transplant? 87. Where is the body’s molecular clock and how does it work? 88. What is the activation synthesis theory? 89. What is reverse learning theory? 90. What is memory consolidation theory and evidence for it? 91. What are the correlations between REM sleep and learning? 92. What is the correlation between REM sleep and behavioral performances? 93. What is the correlation between REM sleep deprivation and memory? 94. What types of learning are not affected by REM sleep deprivation? 95. What is insomnia? 96. What is sleep apnea? 97. What are periodic limb disorder movements? 98. What is narcolepsy? 99. What is REM sleep without atonia? 100. What role does orexin play?
