Neurobiology of Memory and Classic Cases Flashcards
(36 cards)
1
Q
Atkinson & Shiffrin (1968)
A
- Proposed information flows through sensory form, into short-term storage and then short-term memory
- Sensory information is subject to decay (disappear if due to lack of attention)
- Storgae of sensory information is only possible through attention and then stored in short-term storage
- Information is pushed out of short-term storage by more information or rehearsed and retained in long-term storage
- Long-term storage is lost due to interference - confuse information with other information
2
Q
Warrington and Shallice (1969) - Patient K.F
A
- Brain damage demonstrated certain incompatibilities with Atkinson and Shiffrin (1968) model
- K.F had a digit span of 2 (normal is 6-8 items)
- Difficulty in short-term storage but was able to remember long-term information
- Had normal learning abilities
- The idea of flow from short-term storage to long-term storage is incompatible with K.F
3
Q
H.M patient overview
A
- Epiletic who had left and right medial temporal lobes removed: bilateral medial temporal lobectomy
- His seizures were dramatically reduced but so was his long-term memory
- Experienced both mild retrograde amnesia and severe anterograde amnesia
- While H.M was unable to form most types of new long-term memories (LTM), his short-term memory (STM) was intact and also had procedural memory.
4
Q
Retrograde amnesia
A
- Unable to remember the past (before H.M surgery)
5
Q
Anterograde amnesia
A
- Unable to form new memories
6
Q
Assessing H.M - Short Term Memory
A
- Digit Span
- If he was asked to read a series of number, he could repeat them back in order, providing that the time between them being read to him and him having to repeat them back was within a duration of short-term memory (immediate essentially)
- H.M. could repeat digit provided time between learning and recall is within the duration of STM i.e. Immediate recall
- Block-tapping memory-span test
- Demonstrated H.M STM fucntion was good for spatial information - with immediate recall
- Short-term/working memory okay for both verbal and visual spatial information
7
Q
Assessing H.M - Long Term Memory
A
- Digit Span: does not benefit from repeated testing
- Block-tapping memory-span test: does not benefit from repeating testing
- Suggesting amnesia is global, not limited to one sensory modality when it comes to LTM
8
Q
Evidence of new learning - H.M patient tasks
A
- Mirror tracing
- Rotary pursuit
- Incomplete pictures
9
Q
Evidence of new learning H.M - Mirror Tracing
A
- Required to trace between two lines, an outline of an image. Difficult to do when you can’t see what you’re drawing or where your pencil is, except through feedback from a meter
- H.M. was able to do this task with some effort and then showed improvement after a number of trials
- When H.M. came back and was tested again and again, he wasn’t starting at baseline. He had learned and was producing less errors and took less time than he had the first time, performance improved over the course of the day.
- So he was performing and learning this new skill normaly, so retained that learning.
10
Q
Evidence of new learning H.M - Pursuit rotor task
A
- You have to keep a stylus on a rotating target.
- He could also do that and improved over a learning trial period
- HM cerebellum was not damaged by the operation that might be of importance.
11
Q
Evidence of new learning H.M - Incomplete pictures task
A
- Shown a series of images that are in a degraded form. So they’re just basic outline shapes that you didn’t really know what this is.
- Then you’re showing them again and again until a point at which you can identify them and then for those that you’ve been unable to identify your shown more until you can’t identify them.
- Then people are showing them again and can identify them at a lesser stage because they’ve been exposed to them before
- He’s making a number of errors when seen in the degraded forms and less errors when he’s being shown the fuller forms and then when he is retested he’s making fewer errors on the very degraded form, so he’s making more identification and then fewer errors and the second most degraded forms and so on.
12
Q
Scientific contributions of H.M.’s case
A
- Medial temporal lobes are involved in memory
- STM and LTM are distinctly separate - H.M. Is unable to move memories from STM and LTM, a problem with memory consolidation
- Double dissociation with K.F.
- Memory may exist but not be recalled - as when H.M. exhibits a skill he does not know he has learned (dissociation between explicit and implicit memory
13
Q
Episodic and semantic Memory
A
- Unlike episodic memory, semantic memory does not involve conscious recollection of the past
- Extent of amnesia effects on each is different
- Episodic memory generally suffers more greatly (e.g., Spiers et al., 2001; Tulving, 2002; Vargha-Khadem et al., 1997)
- But some patients show more specifically semantic memory deficits (e.g., Yasuda et al., 1997)
- Different involvement of brain areas during encoding and retrieval (Wheeler et al., 1997)
14
Q
Autobiographical Memory
A
- A double dissociation between impairments of personal and semantic memory has been observed (Dalla Barba et al., 1990; De Renzi et al., 1987; Hodges & McCarthy, 1993)
- Neuroimaging data suggest that:
- Visual imagery and emotion centres in the brain, as well as frontal areas involved in self-referential processing, are important for autobiographical memories (Cabeza et al., 2004; Conway et al., 2003; Greenberg et al., 2005)
15
Q
Amnesia: A Modal Model
A
- Baddeley (see 2001) summarised a ‘modal model’ that accounted for most of the findings:
- Episodic memory learning involves associating items with their context using ‘mnemonic glue’ to tie episodes to context
- Recall and recognition involve the same underlying storage processes
- Semantic memory built from episodic memory
16
Q
A Problem for the Modal Model of Amnesia?
The case of Jon
A
- Developmental amnesia due to premature birth and anoxia (deprived of oxygen), which resulted in specific, severe hippocampal damage
- Memory problems appeared obvious from age 5
- However, above average intelligence, good semantic memory
- Impaired recall, but largely intact recognition
- Does not retain or experience episodic memories and the idea that these episodic memories accumulate to create a semantic representation that just doesn’t seem to account for John.
- With double dissociations and the different temporal gradients, it seem to be evidence for dissociable, episodic and semantic systems within long-term memory
- Jon highlights is the importance of the hippocampus in episodic memory
17
Q
Effects of Cerebral Ischemia on the Hippocampus and Memory
A
- R.B patient is a consequence of an operation that went wrong. He had cerebral ischemia (his brain wasn’t supplied with blood, which damages cells).
- R.B. suffered damage to just one part of the hippocampus (CA1 pyramidal cell layer) and developed amnesia
- R.B.’s case suggests that hippocampal damage alone can produce amnesia
- H.M.’s damage – and amnesia – was more severe than R.B.’s
18
Q
Amnesia after Concussion: Evidence for Consolidation
A
- Posttraumatic amnesia
- Concussions may cause retrograde amnesia for the period before the blow and some anterograde amnesia after
- The same is seen with comas, with the severity of the amnesia correlated with the duration of the coma
- Period of anterograde amnesia suggests a temporary failure of memory consolidation
19
Q
Gradients of Retrograde Amnesia and Memory Consolidation
A
- Concussions disrupt consolation (storage) of recent memories
- Hebb’s theory - memories are stored in the short term by neural activity
- Interference with this activity prevents memory consolidation. Examples:
- Blows to the head (i.e., concussion)
- ECS (electroconvulsive shock)
- A blow to the head produces coma
- When victim regains consciousness there is a period of confusion
- When confusion ends, the victim has retrograde emnesia for events that occured before blow and anterograde amnesia for events that occured during confusion
20
Q
The Hippocampus and Consolidation
A
- Proposal that the hippocampus stores memories temporarily (standard consolidation theory)
- Consistent with the temporally graded retrograde amnesia seen in experimental animals with temporal lobe lesions
- Or, perhaps the hippocampus is involved in establishing memories, but they become “stronger” and less dependent on hippocampus over time
21
Q
Neuroanatomy of Object-Recognition Memory
A
- Early animal models of amnesia involved implicit memory i.e recognition memory and assumed the hippocampus was key
- 1970s – monkeys with bilateral medial temporal lobectomies show LTM deficits in explicit memory, the delayed nonmatching-to-sample test
- Like H.M., performance was normal when memory needed to be held for only a few seconds (within the duration of STM)
22
Q
Delayed non-matching-to-sample test for monkeys
A
- Monkey is presented with an object and underneath the object is food and after a delay/ distraction
- The monkey then has two objects, one of which it saw before with food underneath it, and then also an unfamiliar one and in order to get a food reward, it has to recognize that it’s seen an object before and not use that object.
- But instead, look to the unfamiliar object in order to get food.
- In monkeys that didn’t have these bilateral medial temporal lobectomies, they can learn this task quite quickly. And in fact, when they were given lobectomies, they could perform this task initially as well. So when there was only a very brief interlude and no destruction than monkeys could do the task.
- But if you put in delays or even just a minute or so, if you had the distraction, then the demonstrated impairments (couldn’t go for unfamiliar object)
23
Q
Object-Recognition Deficits and Medial Temporal Lobectomy
A
- Neuroanatomical basis of resulting deficits:
- Bilateral removal of the rhinal cortex consistently results in object-recognition deficits
- Bilateral removal of the hippocampus produces no or moderate effects on object recognition
- Bilateral removal of the amygdala has no effect on object recognition
- An explicit memory is being tapped and affected by surgery to the medial temporal cortex
24
Q
Hippocampus and Memory for Spatial Location (Morris water maze)
A
- Rats placed in pool filled with milky water
- Hidden platform that allows the rats to escape
- Healthy rates learn quickly where the platform is and swim directly to it, and are faster at learning on similar tasks
- Rats with hippocampal lesions never learn where the platform is and show no benefit on similar tasks
25
Hippocampus and Memory for Spatial Location
* The rhinal cortex plays an important role in object recognition.
* The hippocampus plays a key role in memory for spatial location
* Hippocampectomy produces deficits in Morris maze and radial arm maze performance.
* Many hippocampal cells are place cells, responding when a subject is in a particular place (and to other cues).
* Grid cells are also found in the entorhinal cortex.
26
Brain structure that supports learning
Amygdala
27
Classical Conditioning
* Amygdala is linked to different types of learning
* Classical conditioning changes the response of neurons to the conditioned stimulus and that change and neuron response is mediated by long-term potentiation
* We can see that when we inhibit long-term potentiation in the amygdala. Or lesion, the amygdala can inhibit classical conditioning
* Hippocampus is broadly understood to be instrumental in learning and memory
28
Hebb (1949)
* Proposed that changes in synaptic efficiency are the basis of LTM
* Long-term learning comes about from cell assemblies (creation of links between cells and groups of cells and the building of relationships) thought to occur when cells are excited at the same time and that excitation can be communicated between them
* Simultaneous excitation of two or more cells
* “neurons that fire together wire together”! - establishment of connection through excitation that will give you a long-term relationship
29
Synaptic Mechanisms of learning and memory
* Long-term potentiation (LTP) is consistent with the synaptic changes hypothesized by Hebb.
* Synapses are effectively made stronger by repeated stimulation.
* LTP can last for many weeks.
* LTP only occurs if presynaptic firing is followed by postsynaptic firing.
30
LTP as a Neural Mechanism of Learning and Memory
* Required intervention where they would place an electrode into an axon of cells that were terminating on cells of interest and the dentate gyrus of the rat
* Elicited by High-Frequency Electrical Stimulation of Presynaptic Neuron; Mimics Normal Neural Activity
* LTP effects are greatest in brain areas involved in learning and memory.
* Learning can produce LTP-like changes.
* Much indirect evidence supports a role for LTP in learning and memory.
* Observation of Associative LTP
* LTP can be viewed as a three-part process.
* Induction (learning) - is when the stimulation and the associated processes happen that create the long-term potentiation
* Maintenance (memory) - changes that happen in the cells
* Expression (recall) - underlie the altered response in the cells
31
Induction of LTP: Learning
* Requires activation of the synapses and depolarization of the postsynaptic neuron, so excitatory transmission where it is mostly studied in the hippocampus - occurs largely through glutamate receptors, AMPA and NMDA receptors
* Most Commonly Studied Where NMDA Glutamate Receptors Are Prominent
* NMDA receptors do not respond maximally unless glutamate binds and the neuron is already partially depolarized. - for NMDA receptors to respond maximally. And so that would be their peak response and allow calcium ions to flood into the cell.
* The glutamate has to bind to these receptors on the postsynaptic membrane has to be depolarized enough in order to displace magnesium ions that are otherwise clogging up the NMDA channels.
* Ca2+ channels do not open fully unless both conditions are met.
* Two requirements:
* Glutamate has to bind
* Depolarization of the cell has to be present
32
When does Ca2+ occur
* If there is the co-occurrence that is needed for LTP, leading to the binding of glutamate at an NMDA receptor that is already depolarized.
33
Ca2+ influx may activate
* Protein kinase C
* And CaM-KII
* that induce changes, causing LTP.
34
Explain this image:
* The influx of calcium ions through the channels and the NMDA receptors.
* When that happens it triggers then an action potential in the postsynaptic neuron.
* So you can see the difference in this image. And a cell that is not depolarized.
* The NMDA receptors are not allowing the calcium ions to come in.
* In a cell that is depolarized, then more calcium is enabled to come through the channels.
* There's just more space and the large numbers of calcium ions that come in, they activate protein kinases (essentially enzymes are activated) and they strengthen existing AMPA receptors.
* Enables more AMPA receptors to be insert
35
Maintenance and Expression of LTP: Storage and Recall
* Long-term changes occur in the Pre- and Postsynaptic Changes
* LTP is only seen in synapses where it was induced.
* Protein synthesis (structural changes) underlies long-term changes. - can increase the number of synapses and can change the membrane as well of the pre- and postsynaptic membranes
* LTP begins in the postsynaptic neuron, which signals the presynaptic neuron.
* How are presynaptic and postsynaptic changes coordinated?
* Nitric oxide synthesized in postsynaptic neurons in response to Ca2+ influx may diffuse back to presynaptic neurons.
* Structural changes are now a well-established consequence of LTP.
36
Variability of LTP
* Fundamental to our understanding of these proposed cell assemblies that have put forward can happen.
* Most LTP research has focused on NMDA-receptor–mediated LTP in the hippocampus, but LTP is mediated by different mechanisms elsewhere.
* LTD (long-term depression) also exists - response to where there's ongoing and repeated low-frequency stimulation from presynaptic neurons that has a different effect
* Much of LTP and the neural basis of memory is still a mystery, despite many research discoveries.
