CH 11: Learning, Memory & Amnesia Flashcards
1
Q
List the 4 specific memory tests used to assess H.M.’s anterograde amnesia.
A
- Digital Span +1 Test
- Block-Tapping Memory-Span Test
- Mirror-Drawing Test
- Incomplete-Pictures Test
- Pavlovian Conditioning
2
Q
Describe the Digital Span +1 Test - what did it test?
A
- Digital Span +1 Test:
- Repeat 5 digits revealed to him at 1s intervals
- -> Then add 1 new digit at end
- Tests verbal long-term memory
3
Q
Describe the Block-Tapping Memory-Span Test - what did it reveal?
A
- Block-Tapping Memory-Span Test:
- Tap array of 9 blocks in front of him in same sequence as the tester did
- Showed that his amnesia not restricted to verbal memory
4
Q
Describe the Mirror-Drawing Test - what did it reveal?
A
- Mirror-Drawing Test:
- Draw line w/in boundaries of target
- -> Repeat over 3 days
- -> Got better each time
- -> Indicates retention of task but didn’t remember actually doing task before
- Showed that his anterograde amnesia didn’t involve ALL long-term memories
5
Q
Describe the Incomplete-Pictures Test - what did it reveal?
A
- Incomplete-Pictures Test:
- Showed HM form new long-term memories
6
Q
Describe the Pavlovian Conditioning.
A
- Pavlovian Conditioning
- Hear tone just before puff of air admin to eye
- Repeat until tone alone elicited an eye blink
7
Q
Describe the 1st major scientific contribution of H.M.’s case.
A
- Showed that the medial temporal lobes play important role in memory
- Challenged previous view that memory functions diffusely throughout brain
- ^Research to relate individual brain structures to specific mnemonic (memory-related) processes
8
Q
Describe the 2nd major scientific contribution of H.M.’s case.
A
- Bilateral medial temporal lobectomy abolished ability to form certain kinds of long-term memories w/o disrupting performances on tests of short-term memory or remote memory
- Support theory that there’s diff models of storage for short-term, long-term & remote memory
9
Q
Describe the 3rd major scientific contribution of H.M.’s case.
A
- Reveals that an amnesic patient may claim no recollection of a previous experience while demo memory for it via improved performance
- Ppl w/ amnesia lose ability to form explicit memories while maintaining ability to form implicit memories
10
Q
Distinguish b/w EXPLICIT memories & IMPLICIT memories.
A
- EXPLICIT Memories = conscious long-term memories
- IMPLICIT Memories = memories that are expressed w/o conscious awareness
11
Q
Describe MEDIAL TEMPORAL LOBE AMNESIA.
What are its major features?
A
Medial Temporal Lobe Amnesia:
= Amnesia ass. w/ bilateral damage to medial temporal lobes
- Its major features = anterograde & retrograde amnesia for explicit memories, w/ preserved intellectual functioning.
12
Q
What has research on Medial Temporal Lobe Amnesia taught us about learning & memory?
A
- Assess implicit memory via REPETITION PRIMING TESTS = seeing list of words, then given fragments of those words & asked to fill in the blanks
- -> Amnesic complete them well despite having no explicit memory of seeing the original list
- -> Discovery of 2 memory systems = explicit & implicit
13
Q
Describe the difference b/w SEMANTIC & EPISODIC memories.
A
Explicit long-term memories come in 2 varieties:
- SEMANTIC Memories = explicit memories for general facts/info
- EPISODIC Memories = explicit memories for particular events of one’s life
- ppl w/ Medial Temporal Lobe Amnesia have difficulty w/ episodic memories
- -> aka have trouble remembering specific life events even though memory for general info is normal
14
Q
Describe GLOBAL CEREBRAL ISCHEMIA.
A
- The interruption of blood supply to entire brain
- Often suffers from Medial Temporal Lobe Amnesia
15
Q
Describe TRANSIENT GLOBAL AMNESIA.
A
- Sudden onset of severe anterograde amnesia & moderate retrograde amnesia for explicit episode memory that’s transit (= only last b/w 4-6hr)
- Occurs in otherwise normal adults
16
Q
Describe the case of R.B..
A
- Underwent cardiac bypass surgery but suffered brain damage bc pump circulating his blood to body while heart was disconnected broke down
- -> Obvious brain damage was restricted largely to the PYRAMIDAL CELL LAYER or just 1 part of the hippocampus - CA1 SUBFIELD
- -> Suggested that hippocampal damage can prod Medial Temporal Lobe Amnesia
- RB suffered Transient Global Amnesia
- -> Abnormalities to the CA1 subfield of the hippocampus
- -> Its sudden onset suggested it was stroke-induced
17
Q
Describe KORSAKOFF’s SYNDROME - describe its symptoms.
A
Korsakoff’s Syndrome:
= Memory disorder common in ppl who have consumed ^^alcohol
Advanced stages characterized by:
- Sensory & motor problems
- Extreme confusion
- Personality changes
- Risk of death from liver, GI or heart problems
- Amnesia here is similar to Medial Temporal Lobe Amnesia
- -> ie) Early stages = anterograde amnesia for explicit episodic memories
- -> However as disorder progresses, retrograde amnesia also develops
18
Q
Describe the etiology of the amnesia of Korsakoff’s syndrome.
A
- Attributable to brain damage ass. w/ thiamine deficiency which accompanies heavy alcohol consumption
19
Q
Describe the symptoms & amnesia effects of Alzheimer’s Disease (AD).
A
Alzheimer’s Disease (AD):
= Progressive disorder w/ mild deterioration of memory until dementia develops
–> so severe patient incapable of simple activities
–> terminal
Pre-dementia patients:
- Major anterograde & retrograde deficits in tests of explicit memory
- Deficits in short term memory & some types of implicit memory
20
Q
Describe the etiology of the amnesia of AD.
A
- ^Reduced levels of acetylcholine
- -> Degeneration of basal forebrain = main source of acetylcholine
–> **Acetylcholine depletion = cause of Alzheimer’s dementia
- But acetylcholine is NOT only factor!
- -> Brain damage is ^^diffused
21
Q
Define POST-TRAUMATIC AMNESIA.
A
- Amnesia produced by a non-penetrating head injury (=blow to head w/o penetrating skull)
22
Q
Summarize the effects of a closed-head injury on memory (3).
A
- A blow to head produces coma
- When victim regains consciousness, there’s a period of confusion
- When period of confusion ends, victim has retrograde amnesia for events that occurred during the period right before the blow to head, & anterograde amnesia for events that occurred during period of confusion
23
Q
Define MEMORY CONSOLIDATION.
A
- Storage of older memories have been strengthened
24
Q
Describe the classic view of memory consolidation.
A
CLASSIC VIEW - Hebb:
- Memories are stored in short term by neural activity reverberating in closed circuits
- -> Circuits susceptible to disruption (ie. blow to head)
- -> Eventually induce structural changes in involved synapses
- -> Provides stable long-term storage
25
Describe ECS.
- ECS = Electroconvulsive Shock = controlled method of studying memory consolidation
- -> Disrupt neural activity
- -> Erase from storage only those memories that hadn't yet been converted to structural synaptic changes
- -> Length of time of retrograde amnesia produced by ECS = estimated time needed for memory consolidation
26
Describe the CURRENT view of memory consolidation.
CURRENT View:
- Memory consolidation continues for a very long time
- Evidence indicates that lasting memories become more & more resistant to disruption throughout one's life
- Each time a memory's activated, it's updated & linked to additional memories
- -> These additional links ^ the memory's resistance to disruption by cerebra trauma (ie. concussion or ECS).
27
Describe the DELAYED NONMATCHING-TO-SAMPLE TEST.
How would normal monkeys perform vs. those w/ bilateral medial temporal lobe lesions?
What did this test provide a means for testing?
Delayed Nonmatching-to-Sample Test:
- Subject presented w/ unfamiliar sample object
- -> After delay, is presented w/ choice b/w sample object & unfamiliar object
- -> The correct choice is the unfamiliar object (bc monkey would get i.e. food reward ass. w/ unfamiliar object)
- Normal monkeys would perform correctly, whereas those w/ bilateral medial temporal lobe lesions had major object-recognition deficits
- This test provided a means of testing the assumption that amnesia resulting from medial temporal lobe damage is entirely consequence of HIPPOCAMPAL damage**
- Bc of size & location of hippocampus, all studies of hippocampal lesions in monkeys involved ASPIRATION (suction) of large portions of medial temporal cortex, in add. to hippocampus
- But in RATS: damage ass. w/ aspiration lesions of hippo limited to small area of parental neocortex
- -> also rat lesion small enough it can be lesioned electrolytically or w/ neurotoxin injections
- -> Prod less extraneous damage
28
Describe the neuroanatomical basis for the object-recognition deficits that result from bilateral medial temporal lobectomy.
- Hippocampus plays key role in object-recognition memory
> SUPPORT:
- Object recognition memory is ^^disrupted by medial temporal cortex lesions, but only moderately by hippocampal lesions
- Relation b/w ischemia-produced hippocampal damage & object-recognition deficits in humans, monkeys & rats
- Damage to brain structures other than hippocampus contributes to amnesia observed in patients w/ global cerebral ischemia
- -> Hippo damage following global cerebral schema = damage to CA1 subfield of hippo
29
Describe hippocampal PLACE CELLS.
Place Cells:
= Neurons that respond only when the subject is in specific location (i.e. in the place field of the neurons)
- ie) when rat placed in unfamiliar environment, none of its hippocampal neurons have a place field in that environment
--> Then rat familiars itself w/ environment
--> Many hippo neurons acquire a place field in it
--> aka each fires only when rat is in a particular part of the environ
-** Each place cell has a place field in a diff part of the environ
30
Describe the ENTORHINAL CORTEX.
- Area of medial temporal cortex that's a major source of neural signals in hippocampus
31
Describe entorhinal GRID CELLS.
Grid Cells:
- Entiorhinal neurons that have an extensive array of evenly spaced place fields, producing a pattern reminiscent of graph paper
32
Describe the relationship b/w hippocampal Place Cells & entorhinal Grid Cells.
- Hippo place cells depend on input from entorhinal grid cells:
(1) There's a major pathway from entorhinal cortex to hippo
(2) Entorhinal grid cells respond relatively reflexively to location, whereas hippo place cells respond to place in combo w/ other features of environ
- Hippocampal place cells obtain their spatial info via grid cells in entorhinal cortex
- -> This even spacing of the place fields in the grid cells could enable spatial computations in hippocampal place cells
- Place cells can still function after entorhinal grid cells have been eliminated
33
Describe the role of the hippocampus in spatial memory & other types of memory it supports.
1. Certain cells in hippo shown to code for TEMPORAL aspects of an experience
2. Hippo plays role in learning about social organization in humans
3. Cells in hippo & its surrounding structures shown to play role in coding of concepts
34
List 3 amor structures of the Medial Temporal Lobes.
1. Hippocamps
2. Amygdala
3. Medial Temporal Cortex = entorhinal, peripheral & parahippocampal cortices
35
Define a CONCEPT CELL.
Concept Cells:
= neurons, such as those found in medial temporal lobe, that respond to ideas/concepts rather than to particulars
- Highly selective
- -> Each neutron responded to only a small # of test objects/indiv
- -> Each neutron responds to >1 concept, but there's usually an obvious relation b/w them
- aka Jennifer Aniston Neurons
36
Explain what an ENGRAM CELL is.
Engram Cells:
= Neurons that maintain an engram
- Engram = hypothetical permanent change in brain, accounting for the existence of memory
37
Describe what OPTOGENETICS is.
- Neuroscientists insert an opsin gene into a particular neuron
- -> Use light to hyperpolarize/depolarize those neurons
38
Describe how Engram Cells were identified using Optogenetics.
(1) Tagging Stage:
- Neurons active during learning task are induced to express opsin while animal engages in particular learning task
(2) Manipulate Stage:
- Previously active neurons are now inhibited or excited by using light to influence the actively opsin-tagged neurons
--> Now able to observe, suppress, or activate engram cells in different parts of NS
**see pg 291-292**
39
List the types of memories that are stored in: INFEROTEMPORAL CORTEX.
Inferotemporal Cortex:
= Cortex of the inferior temporal cortex
- Important role in storing memories of VISUAL input
40
List the types of memories that are stored in: AMYGDALA.
Amygdala:
- Plays special role in memory for the emotional significance of experiences
- Little evidence that it STORES memories
- -> Involved in strengthening the emotional significant memories stored in other structures
- -> May be why emotionally-provoking events are remembered better than neutral events
41
List the types of memories that are stored in: PREFRONTAL CORTEX.
Prefrontal Cortex:
= Area of frontal cortex anterior to motor cortex
- Patients w/ damage to prefrontal cortex display no deficits on conventional memories tests
- -> BUT 2 episodic memory abilities are often lost by patients w/ large prefrontal lesions:
(1) Anterograde & retrograde deficits in memory for temporal order of events, even when they can remember the events themselves
(2) Deficits in working memory
- -> Thus patients have difficulty performing tasks that involve series of responses
- Specific complex patterns of prefrontal activity ass. w/ various memory functions
42
List the types of memories that are stored in: CEREBELLUM.
Cerebellum:
- Storage of memories of learned sensorimotor skills.
- Plays role in certain types of memory w/ no obvious motor component
43
List the types of memories that are stored in: STRIATUM.
Striatum:
- Storage of memories for consistent relationships b/w stimuli & responses
- -> The type of memories that develop incrementally over many trials
- Plays role in certain types of memory w/ no obvious motor component
44
Describe the phenomenon known as LONG-TERM POTENTIATION (LTP).
What are LTP's 2 key properties proposed as characteristics of physiological mechanism of learning & memory?
Long-Term Potentiation (LTP):
= The enduring facilitation of synaptic transmission that occurs following activation of synapses by high-intensity, high-frequency stimulation of presynaptic neurons
- Most frequently studied in the rodent hippocampus
Key Properties:
(1) LTP can last for a long time
- Several months after multiple high-frequency stimulation
(2) LTP develops only if firing of the presynaptic neuron is followed by firing of postsynaptic neuron
45
Provide evidence that LTP is related to neural mechanism of learning & memory (8).
1. LTP can be elicited by low levels of stimulation that mimic normal neural activity
2. LTP effects are most prominent in structures implicated in learning & memory (i.e. hippocampus)
3. Learning can produce LTP-like changes in hippocampus
4. Many drugs that influence learning & memory have parallel effects on LTP
5. Induction of maximal LTP blocks the learning of a Morris water maze until the LTP has subsided
6. Mutant mice displaying little hippocampal LTP have difficulty learning Morris water maze
7. Behavioural changes that appear to be memories can be induced in mice via LTP
8. LTP occurs at specific synapses shown to participate in learning & memory in simple invertebrate NS's
**see pg 294-295**
46
***FINISH LO 11.18 - 11.22***
do it...
