26. Optical illusions can only be demonstrated in people since it requires someone to report what they see. Correct?

false; in class we had seen a video in which the dogs would avoid the rug because it seemed like they were going to fall in a hole.

29. What are Duchenne and non-Duchenne smiles?

a duchenne smile is someone's natural smile without forcing it which is non duchenne.

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Psych Learning

Question	Answer
1. What are the CS, US, CR and UR in the Miller Lite ad shown in class?
2. What is hybrid classical/operant conditioning and how might it develop?
3. Bosco was trained to ring a bell to go outside. Describe how the training involved classical conditioning (what were the CS, US, CR, UR) and how did the behavior transition to operant conditioning?
4. Bosco was trained so that “the hand” signal meant he wouldn’t get food. What were the CS, US, CR, UR?”
5. What is shaping? How might it happen in someone’s daily life? How might it be used to train a dog?
6. What is “vicarious reinforcement”?
7. What is an example of partial reinforcement and why is it more difficult to extinguish than continuous reinforcement?
8. What general category of behavior is erroneous CS-US pairing and how does it develop into operant conditioning?
9. What is the fundamental difference between classical and operant conditioning?
10. In what way are primates different from other animals in terms of stress?
12. What is the incidence of cancer versus cardiovascular disorders in people with PTSD? Why?
13. Which 2 emotional components of the Type A personality put a person at increased risk of a heart attack? Which component of the Type A personality does not put a person at increased risk of a heart attack?
14. Why is it so difficult to extinguish conditioned fear after someone is traumatized?
15. What is the difference between an Unconditioned Stimulus (US) and a secondary reinforcer in the classical conditioning terms covered in class?
16. What is sensory preconditioning and how was it illustrated in class?
17. A radar police car is sometimes immediately behind a sign, which is in front of a tree, which is in front of a fire station. What could be the CS’s, RS, CR and RR? Why would the CR be resistant to extinction?
18. A man is attacked by a large dog in the evening while he was jogging in the park.
a. What are the US, CR and UR?
b. Name 3 different stimuli that can be considered the CS.
c. How might you conduct extinction conditioning to help him recover?
19. a. In Watson’s study of Little Albert, what were the CS, US, CR, UR?
b. In Watson’s study how was CS generalization assessed?
20. In terms of the “best stimulus” how does image processing by single cells change from the retina to visual cortex to inferior temporal cortex (of monkeys) to the human hippocampus?
21. Why is it so easy to produce optical illusions?
22. What is the finding presented in class that auditory and visual perceptual plasticity can occur rapidly and then persists?
23. What is the evidence that a single brain cell can “represent” a person? What is a grandmother cell?
24. What is inattentional blindness? How was it demonstrated in class? How does it relate to parietal cortex damage and unilateral neglect?
25. How does inattentional blindness relate to how stress affects perception
26. Optical illusions can only be demonstrated in people since it requires someone to report what they see. Correct?	false; in class we had seen a video in which the dogs would avoid the rug because it seemed like they were going to fall in a hole.
27 What are the 4 approaches that demonstrated the importance of the inferotemporal cortex in higher cognitive functioning?
28. Describe the 3 observations by Darwin regarding non-verbal communication.
29. What are Duchenne and non-Duchenne smiles?	a duchenne smile is someone's natural smile without forcing it which is non duchenne.
30. Which ban areas generate the Duchenne and non-Duchenne smiles?
31. How might strokes in each of the two areas from question 30 be expressed?
32. How was eye contact as a form of non-verbal communication expressed in 2 recent presidential debates?
34. Why would someone with an autoimmune disease, such as lupus, have their symptoms worsen when they’re under stress?
35. Give 2 reasons why it’s adaptive for the immune system to be stimulated in response to stress.
36. Why do platelets become “sticky” in response to stress? What would be an adverse consequence to this “adaptive” response to stress?
37. a. What study showed that people under stress develop increased epinephrine and increased platelet activation factors?
b. What natural experiment showed that people under stress developed increased platelet activation factors? What was the consequence of this natural experiment?
38. Why is it adaptive to enhance memory formation under stress? What would be the maladaptive consequence to this “adaptive” response to stress?
39. Why do people with PTSD tend to be overweight?
40. Is there evidence of brain damage in people with PTSD? What does it mean for the brain to be dysfunctional versus hyperfunctional, and how does that apply to PTSD?
41. What study on Swiss Subjects demonstrated a link between a gene and emotional memory processing?
42. How did the two forms of the gene influence amygdala responses to arousing images?
43. Did the gene variants affect how strongly people reacted to arousing stimuli?
44. How did the study on Swiss Subjects relate to traumatized people with PTSD in Rwanda?
45. How does the 5-HTT (serotonin) gene interact with early life experience to produce depression in adults?
46. From an evolutionary perspective, why is it adaptive for the PFC to be inhibited in response to stress?
47. Give 4 reasons why people with PTSD have cognitive deficits and one reason why PTSD does not cause cognitive deficits.
48. What is epigenetics?
49. What is methylation and how can it be reversed?
50. a. What is the evidence that links hippocampal size to PTSD susceptibility?
b. Does the hippocampus shrink in size in people with PTSD?
51. How is the balance between the PFC and amygdala shifted in PTSD?
52. What is the laboratory evidence for a link of stress to amygdala activity to inflammation to heart attacks?
53. What is the neurobiological and evolutionary basis for why people with PTSD have impaired sleep.
54. Which risk factor is common to all forms of PTSD?
55. How is neurogenesis affected by stress?
56. Describe the natural experiment in people that showed that damage to the amygdala completely blocks the development of PTSD.
57. Describe the study that showed a triple risk factor (social/genetic/trauma) interaction that produced a high rate of PTSD.
58. Is stress-induced neuronal atrophy permanent? How do we know?
59. What natural experiment revealed that someone’s brain chemistry changes after developing PTSD? Which brain neurotransmitter system changes in PTSD?
60. What is odd about cortisol levels in people with PTSD? How does this unexpected finding fit with the immune system’s response to trauma?
61. Why would cortisol be called the “anti-stress hormone”?
62. Define: dementia, aphasia, apraxia, agnosia
63. Describe the importance of BDNF to brain function and how it is affected by stress.
64. What is another term for “vascular dementia”?
65. Incorrect or Correct: There is a greater incidence of Alzheimer’s disease now because in the past people died at a young age, before they could develop Alzheimer’s disease.
66. Incorrect or Correct: Alzheimer’s disease is an inevitable consequence of aging.
67. Incorrect or Correct: When cognitive disorders in Alzheimer’s disease develop they begin with damage at the lowest brain areas, such as the hypothalamus, and slowly progress upward to the hippocampus and neocortex.
68. Incorrect or Correct: High cholesterol is associated with a greater incidence of dementia in Alzheimer’s diseases.
69. a. Describe and evaluate the “Cognitive Reserve” hypothesis of Alzheimer’s disease.
b. What was the evidence in favor of the Cognitive Reserve” hypothesis and what was the explanation for it provided in class?
70. Name 5 risk factors associated with the development of Alzheimer’s disease.
71. Which Apolipoprotein gene allele has a high association to the development of Alzheimer’s? Is Alzheimer’s disease inevitable if a person has this gene?
72 What evidence is there that APOE4-related cognitive deficits can be reversed?
73. a. What single factor in the diet is associated with Alzheimer’s?
a. What single factor in the blood is associated with Alzheimer’s?
74. What evidence in people relates reduced brain glucose utilization to Alzheimer’s?
75. How might the BBB be related to the development of Alzheimer’s?
76. Why might consumption of coconut oil reverse the development of Alzheimer’s disease?
77. How is lifespan calculated? Evaluate the statement: People died too young in 1900 to see much Alzheimer’s, cancer or heart disease in the US population. What percent of the adult population in the US in 1900 was over 75 years old?
78. The Pilgrims lived in Massachusetts in the 17th century. Were they known for dying young or old? What was the age of death of one Pilgrim, William Brewster? Is there any documentation of senility or dementia among the Pilgrims?
79. What is the link of fasting blood sugar to dementia? At what level is fasting blood sugar linked to dementia? What is the link of blood sugar to hippocampal size with advanced age?
80. What is the evidence that highly fit people have a very low incidence of dementia?
81. Which blood marker other than glucose is associated with increased risk of Alzheimer’s and heart disease?
82. Evaluate the statement: Elderly people with high cholesterol levels are in greater danger of having heart attacks, strokes, Parkinson’s and Alzheimer’s disease.
83. Are brain training exercises effective at reducing the incidence of Alzheimer’s disease and slowing the rate of brain aging?
84. Describe the interaction between the APOE4 gene with smoking and diabetes in terms of Alzheimer’s risk.
85. Why is Alzheimer’s disease called type 3 diabetes?
86. Under what conditions are ketones produced?
87. What is a “transgenic” animal? How was work on these animals used to study Alzheimer’s disease?
88. What 2 specific measures, related to diabetes, are different in Alzheimer’s disease from healthy brains?
89. What is the evidence that elevated levels of blood sugar contribute to atrophy of the hippocampus with old age?
90. What 2 brain diseases are more common in people with low cholesterol compared to those with high cholesterol?
91. Evaluate the statement: Elderly people with high cholesterol levels are in greater danger of having heart attacks, strokes, Parkinson’s and Alzheimer’s disease.
92. What is the experimental evidence that a person with the APOE 4 gene can have a reversal of cognitive impairment?
93. What two forms of energy can the brain use and which one is used by most people?
94. Elderly people with high cholesterol live longer than people with low cholesterol. True or false
95. What is an alternative to using diet to increase ketones to enhance brain function?
96. Who developed the hypothesis that consumption of animal fat will cause heart disease? Has that hypothesis been supported by research? What is healthier, margarine or butter? Which is recommended by the AHA?
97. a. Is there an association between egg consumption and heart disease?
b. How do eggs affect serum cholesterol?
98. How does adding fat to a meal affect nutrient absorption?
99. Which blood marker is associated with increased risk of Alzheimer’s and heart disease?
100. Evaluate the statement: Elderly people with high cholesterol levels are in greater danger of having heart attacks, strokes, Parkinson’s and Alzheimer’s disease.
101. What is the experimental evidence that a person with the APOE4 gene and metabolic syndrome can have a reversal in the development of cognitive impairment?
102. What two forms of energy can the brain use and which one is used by most American people?
103. Describe the study and outcomes relating cholesterol levels to cognition.
104. Elderly people with high cholesterol live longer than people with low cholesterol. True or false – describe 3 studies on the topic
105. A drug company conducts a study on people with heart disease and finds that 2% of all people given a placebo have a heart attack and 1% of all people given the drug have a heart attack, which is a reduction from 2% to 1% with the drug. How many peopl
106. Which single factor links stress, obesity, smoking, inflammation, hypertension and type 2 diabetes to heart disease and stroke?
107. What is the evidence that statins contribute to the development of a morphological feature of Alzheimer’s disease?
108. Why did President Eisenhower have a heart attack while he was in office?
109. What study demonstrated that statins can produce a dementia-like effect in 75 year old people?
110. Why do some statins have an adverse effect on memory and others don’t?
111. What are three reasons why NMDA receptors get desensitized in phase 2 of the temporal dynamics model?
112. Describe the stress-PB potentiation in vitro study results and what it tells us about how stress affects the brain.
113. Describe the findings that demonstrated that it was cat-induced fear, and not just arousal, novelty or aversiveness, that impaired spatial memory in the rats?
114. How were working and reference memory tested in the rat study on the radial arm maze for food? How did stress affect each kind of memory? What would be an analogous working/reference memory experience for a person? How would you test working and refe
115. How is memory studied in a rat in a way that is analogous to human memory for where you parked your car in the same location every day or when your car is in a different place each day. How would the human hippocampus be involved in the 2 forms of me
116. Describe how 30 minutes of stress versus 2 minutes of stress before learning affected a rat’s 24 hr memory. Why is there a difference in memory effect between the two manipulations?
117. How does stress affect LTP in the amygdala? How do we know that amygdala activity is necessary for stress to impair memory?
118. a. How might subconscious (non-declarative) memory be affected if the learning occurs when the hippocampus is in phase 2?
b. How might conscious (declarative) memory be affected if the learning occurs when the hippocampus is in phase 2?
119. What is the evidence that memory formation occurring while the hippocampus is in phase 1 is enhanced? How does this relate to human flashbulb memory?
120. What finding in traumatized people is consistent with the predictions of the temporal dynamics model of hippocampal memory processing?
121. How would placement of GABA in the Hippocampus affect working compared to reference memory?
122. Which brain structure is activated only briefly to produce fragmented memories in PTSD?

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