High-Yield Physiological Psych

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Lecture 5, 6, and 7

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148 Terms

1
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What are the three distinct memory stores?

Sensory → STM (working) → LTM

2
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What helps sensory memory progress to the next stage?

Attention

3
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What helps working/short-term memory progress to long-term memory?

Consolidation thru repetition

4
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What is the relationship between long-term memory and short-term memory?

Retrieval: long term memories can be reaccessed into STM

5
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What are the two broad divisions of LTM?

Explicit (declarative) and implicit (non-declarative)

6
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What are the two types of declarative (explicit) memory?

Semantic (facts) and episodic (personal experiences)

7
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List types of nondeclarative (implicit) memory.

Procedural memory, priming, classical conditioning

8
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True or false: LTM is unitary

False, it has partially overlapping and partially distinct neurological networks

9
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Who was patient H.M., and what surgery did he undergo?

He had epilepsy, resolved through surgery removing medial temporal lobes

10
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What was H.M.’s main memory deficit?

Anterograde amnesia, cannot consolidate new LTMs

11
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Define anterograde amnesia.

Inability to form new long-term memories

12
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Define retrograde amnesia.

Inability to remember events prior to the brain damage

13
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What happened to H.M.’s short-term memory?

Relatively intact

14
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What did mirror-drawing performance show in H.M.?

Procedural (implicit) memory intact, without remembering doing it prior

15
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What did incomplete-pictures tasks show in H.M.?

Priming (implicit) memory intact, does not remember prior exposure (explicit memory)

16
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What key “dissociation” did H.M. demonstrate?

Explicit (loss) vs implicit (preserved)

17
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What did H.M. teach us about the medial temporal lobes?

They play a key role in memory (especially forming new long-term memories)

18
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What did H.M. teach us about STM vs LTM?

They are distinct systems

19
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What causes Korsakoff’s syndrome?

Deficiency in B1 vitamin (poor diet/nutrition, alcoholism)

20
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How is Korsakoff’s syndrome treated?

Vitamin B1

21
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What is confabulation (as seen in Korsakoff’s)?

Amnesia where you remember past events but in the wrong order

22
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What brain region is typically damaged in Korsakoff’s syndrome?

Medial diencephalon

23
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How does early Korsakoff’s amnesia compare to medial temporal lobe amnesia?

Similar symptoms (as H.M., anterograde amnesia)

24
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What is the general progression pattern of Alzheimer’s disease in the brain?

Will cover the entire cortex within 20+ years (spread from the hippocampus to language areas first)

25
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What is global cerebral ischemia?

Blood flow is restricted from the brain

26
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Which hippocampal region is most vulnerable in global cerebral ischemia?

CA1, most vulnerable = largest exit tract

27
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What type of memory problem can global cerebral ischemia produce?

Anterograde amnesia (similar to H.M.)

28
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Which patient demonstrated anterograde amnesia after CA1 damage from global cerebral ischemia?

R.B.

29
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What types of amnesia can concussions cause?

Retrograde and anterograde amnesia

30
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What do concussion-related amnesia patterns suggest?

Temporary failure to consolidate memories

31
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State Hebb’s theory of memory consolidation.

“Cells that wire together, fire together”

32
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According to Hebb, how are short-term memories stored?

Continuous electrical stimulation (loop) → reverberating neural activity

33
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According to Hebb, how is long-term memory (learning) stored?

Strengthening connections between two synapses = synaptic changes → firing together

34
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What did ECS (electroconvulsive shock) studies with rats demonstrate about consolidation?

Memory consolidation takes time

35
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In ECS studies, what was special about information consolidated within about 3 hours?

It was resistant to disruption (had already been consolidated)

36
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What did long gradients of retrograde amnesia from ECS therapy patient suggest?

Consolidation can continue for up to years

37
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What is reconsolidation theory?

Memories can be retrieved from LTM → STM and be “edited” and reconsolidated that way

38
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What is one implication of reconsolidation theory?

Treating PTSD

39
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True or false: all medial temporal lobe structures have the same role in memory?

False - they play different roles

40
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What is the rhinal cortex important for?

Object recognition

41
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What is the hippocampus important for?

Spatial memory

42
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What are place cells?

Hippocampal cells that fire when entering a specific, familiar environment

43
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When do place cells develop their location-specific firing patterns?

After becoming familiar with an environment

44
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Where are memories stored in the brain?

Diffusely across the brain structures involved in their initial consolidation

45
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What is the hippocampus especially important for regarding memory storage?

Initial consolidation (before its distributed)

46
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What does Hebbian learning say about synapses?

Co-occurrence of pre- and postsynaptic firing strengthens synapses (repeated firing together)

47
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What is long-term potentiation (LTP)?

High-frequency stimulation strengthens a connection → neurons become more responsive to each other over time

48
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What does LTP demonstrate?

Synaptic plasticity (learning-related strengthening of synapses)

49
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In LTP, what happens to EPSPs after high-frequency stimulation?

EPSP responses increase, postsynaptic neuron becomes more likely to respond

50
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Why are NMDA receptors crucial for LTP and learning?

Allow calcium entry when neurons connect → strengthens the synapse

51
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What happens if NMDA receptors are blocked (as seen in rats task learning)?

LTP cannot occur + prevents task learning

52
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Define a brain tumor.

Mass of cells growing independently from the rest of the body

53
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What is a benign brain tumor?

Non-cancerous, does not invade surrounding tissue

54
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What percentage of brain tumors are meningiomas (example of benign)

20%

55
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What is a malignant brain tumor?

Cancerous, aggressive, invasive tumors

56
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What is a metastatic tumor?

Example of malignant, cancerous tumor that is created somewhere else and travels to the brain

57
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What are cerebrovascular disorders?

Blood vessel-related conditions affecting the brain

58
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What is a stroke?

Interruption of blood flow to the brain

59
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What is cerebral hemorrhage?

Bleeding due to bursting blood vessel

60
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Differentiate subarachnoid vs intracerebral hemorrhage.

Subarachnoid (surface), intracerebral (deep)

61
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What is cerebral ischemia?

Block of blood flow to the brain tissue

62
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What is atherosclerosis?

Thickening and becoming less flexible of the arteries

63
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True or false: damage due to cerebral ischemia is immediate.

False

64
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What excitotoxic cascade contributes to ischemic damage?

Lots of glutamate releases → overactivates NDMA receptors → release of Na+ and Ca+ → neuron death

65
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What is the treatment tPA and when must it be given?

Within 3 hours of stroke symptoms, tPA = tissue plasminogen activator (clot buster)

66
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What is a TIA?

Transient ischemic attack (“mini-stroke”)

67
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What are closed-head injuries?

Brain injuries without penetrating wounds (brain colliding with skull)

68
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What are cerebral contusions?

Bruising of the brain, causes damage to the cerebral circulatory system

69
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What is a coup-contrecoup injury?

Injury at impact site, and bounces and injures the opposite side of the impact site

70
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What is a concussion?

Blow/acceleration forces causing the brain to move rapidly inside the skull

71
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What is punch drunk syndrome/CTE?

Repeated head trauma, such as concussions/blows over time (chronic traumatic encephalopathy)

72
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What are cerebral abscesses and how are they treated?

Pockets of pus → antibiotics like penicillin

73
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What does a viral infection affect in the nervous system context?

Neural tissue

74
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Define meningitis.

Inflammation of the meninges

75
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Compare viral meningitis vs bacterial meningitis.

Bacterial is much more severe/deadly

76
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Define encephalitis.

Inflammation of the brain tissue.

77
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What are neurotoxins?

Toxins substances that damage nerve cells (neurons)

78
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How can neurotoxins enter the body?

Inhaled (lungs), ingested (GI tract), absorbed (skin)

79
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Why are organic solvents especially problematic neurotoxins?

They get into the BBB → lipophilic (dissolve thru fats like neurons)

80
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What is Alzheimer’s disease most commonly associated with?

Dementia

81
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Approximately what percent of people over 65 have Alzheimer’s?

10%

82
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Approximately what percent of people over 85 have Alzheimer’s?

35%

83
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What cognitive domains decline in Alzheimer’s disease?

Visuospatial, executive, memory, language

84
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When is Alzheimer’s definitively diagnosed?

Autopsy (observe neurofibrillary tangles and amyloid plaques)

85
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What is Parkinson’s disease?

Neurodegenerative motor disorder

86
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What is the typical early onset age for Parkinson’s?

60 years old

87
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Why is L-dopa used in Parkinson’s treatment?

To penetrate the BBB → turning into dopamine

88
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What treatment is used after L-dopa stops working?

DBS (deep brain stimulation)

89
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Which brain region degenerates in Parkinson’s disease?

Substantia nigra neurons

90
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What is Huntington’s disease?

Genetic neurological disorder causing progressive brain cell death

91
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What is the typical onset age range for Huntington’s disease?

30-50 years old

92
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What gene is mutated in Huntington’s disease?

Huntingtin gene

93
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What is the inheritance pattern of Huntington’s disease?

Autosomal dominant (only one copy needed)

94
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What is chorea?

Dense in greek → describes movements of Huntington’s patients that are involuntary and excessive

95
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What structural brain change is noted in Huntington’s disease?

Enlarged ventricles

96
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What is the main goal of Huntington’s treatment?

Reduce symptoms thru lowering dopamine levels

97
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What is multiple sclerosis?

Autoimmune disease affecting the nervous system, attacks CNS myelin (oligodendrocytes)

98
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Why are early MS symptoms often visual?

Optic nerve is thinner → more vulnerable

99
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Is MS primarily genetic?

No, environment (vitamin D exposure) and virus exposures play a role

100
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What is epilepsy?

Neurological condition, reoccuring seizures

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