03-10-23 - Learning and memory Flashcards

1
Q

Learning outcomes

A
  • Recall classic theories of memory organisation and consolidation with respect to associated cortical and sub-cortical pathways, and the taxonomy of diferent forms of memory.
  • Explain how structural change at synaptic level contributes to learning
  • Explain using clinical examples, the diferent types of cortical or subcortical structural damage resulting in anterograde and retrograde types of memory loss.
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2
Q

What is the definition of memory?

What are engrams?

A
  • Memory is a mechanism by which past experience alters present experiences or behaviours
  • Engrams are the link between memories and remembering
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3
Q

What did the Lashley (1890-1958) experiments show?

What was the implication of these data?

Where are engrams thought to be located?

A
  • Early experiments (Lashley 1890-1958) showed that rats did not form specific pathways between sensory areas and motor areas (early engram idea)
  • His results showed that quite large areas of cerebral cortex had to be removed to prevent learning and memory of complex tasks, and that these lesions had little effect on simple tasks – up to 50% of the brain was removed, and still there were low levels of mistakes in the maze tasks performed
  • The implication of these data are that memory and learning is performed using parallel processing systems and not serial processing systems
  • Currently we think engrams are located all over the brain, but in places related to processing and learning (amygdala for fearful memories etc ) – ie there is not 1 particular area where all memories are kept and there is not a particular pathway that needs to be kept for memories to exist
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4
Q

Hebbian learning and networks

What does Hebbian learning suggest?

What adage does this give rise to?

What is habituation?

What is sensitisation?

A
  • Hebbian learning and networks
  • Hebbian learning suggests as cells fire simultaneously they increase the synaptic associations.
  • This is positive feedback that can grow network stability
  • This results in networks of cells which are synaptically linked - associative learning
  • Hebbian learning gave rise to the adage that ‘cells that fire together, wire together’
  • Habituation is the decrease in response (& NT release) with repeated stimulus (we get used to it)
  • Sensitisation is the increase in response with repeated stimulation – mediated by an interneuron
  • The interneuron (usually) can become more and more active as time goes on meaning we ‘take the breaks off’
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5
Q

What is Long term potentiation (LTD) an example of?

What is LTD?

How does it affect signal transmission between 2 neurons?

A
  • Most typical examples of Hebbian mechanisms are long-term potentiation (LTP), and long-term depression (LTD)
  • Long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity.
  • These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons
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6
Q

Describe the specificity of LTP

In what experiment was this first shown?

How was this experiment set up?

Describe the 5 steps in the rabbit hippocampus experiments (1970s).

What does this experiment demonstrate?

A
  • Long term potentiation (LTP) is path specific
  • This was first shown in rabbit hippocampus experiments (1970s)
  • In this experimental setup, there are 2 neurons with axons going to a 3rd receiving neuron
  • 5 steps in the rabbit hippocampus experiments (1970s):

1) Stimulate pathway 1 with a single spike and record

2) Stimulate pathway 1 with a train of spikes

3) Re-stimulate with a single spike and measure EPSP

4) Stimulate pathway B with a single spike and measure the EPSP

5) Enhanced response in Path 1 is long-lived and specific to that pathway Long term synaptic changes requires genetic involvement

  • This demonstrates if we stimulate a neuron in a particular way, we can increase its response to a particular stimulus -LTP
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7
Q

If synapses were only capable of LTP what would eventually happen?

What is needed to prevent this?

What is LTD (long-term depression) initiated by?

How can LTD affect LTP?

A
  • If synapses were only capable of LTP, this would lead to whole brain potentiation
  • To prevent this, there is a reverse effect called recall habituation (Long term depression – LTD)
  • LTD is initiated by a slower train of stimulatory impulses over a longer period
  • LTD can modulate LTP or even reverse it
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8
Q

What is memory duration used for?

What are 3 types of memory based on duration?

A
  • Memory duration is used to define memory types and processes
  • 3 types of memory based on duration:
    1) Short term memory
    2) Long term memory
    3) Working memory
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9
Q

What are 3 characteristics of short-term memory?

A
  • 3 characteristics of short-term memory?
  • Short term memory is:

1) A very brief memory (seconds) either from an external stimulus or retrieval from a long-term memory

2) Easily displaced by another stimulus

3) Can be extended into working memory by a) repetition in a phonic loop (temporal extension) or b) chunking which links familiar chunks together to extend the size of chunk

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10
Q

What is the most common clinical test for short term memory?

Describe this test.

What is chunking?

A
  • The most commonly used clinical test of short-term memory is the digit span:
  • Subject reads an increasing series of numbers which they immediately repeat
  • The number of digits that can be repeated back immediately is the digital span. - Usually around 6-7 digits is normal
  • If you already know several sequences, you can simply remember which sequences to recall – called ‘chunking’ & is used by chess masters
  • i.e. the twelve letters U,I,S,A,B,S,M,C,P,D,O,F are easy when they are ‘chunked’ into USA, IBM, SCO, PDF
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11
Q

What are 2 characteristics of working memory?

How can working memory be described in terms of short-term memory?

What occurs when a working memory task is completed?

What is another way for long term memory (LTM) to be formed?

A
  • 2 characteristics of working memory:
  • Working memory is:

1) The maintenance and integration of information in an active state for a relatively brief time in order to achieve a short-term task or goal

2) Is comprised of a mixture of short and/or retrieved long term memory

  • As short-term memory only lasts a few seconds it must be repeatedly re-activated, its reactivation and subsequent duration is working memory (this is known as an executive function).
  • When the task is over, the working memory either is encoded into long term memory or is left to lapse
  • Note that it is also possible for LTM (long-term memory) to be formed directly from sensory input under control of executive functions (pre-frontal cortex)
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12
Q

What is LTM?

How large is LTM compared to working memory?

What are the 2 sub-divisions of LTM?

A
  • Long term memory (LTM) is the acquisition and retrieval of information over long periods
  • Long term memory (LTM) is huge in comparison to working memory
  • 2 sub-divisions of LTM:
    1) Declarative memory
    2) Non-declarative memory
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13
Q

Describe the flow chart for declarative/explicit LTM (in picture)

A
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14
Q

Describe the flow chart for implicit/non-declarative LTM (in picture)

A
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15
Q

What parts of learning and memory are context dependent?

What does the process of learning (storing memory) consist of?

A
  • Sub divisions of both learning and memory are context dependent e.g joy of eating dish and chips on Friday night – all memories are flavoured with the limbic system i.e remembering the joy/smell of the memory
  • Despite these different sub divisions, the process of learning (storing memory) is thought to be similar to all types and consists of 4 parts:

1) Encoding (memory creation)

2) Storage (persistence of memory traces)

3) Retrieval (memory recovery)

4) Consolidation (strengthening of memory traces)

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16
Q

Label these structures associated with the formation of memory in the temporal lobe system (in picture)

A
17
Q

Describe the 3 steps in memory formation.

A
  • 3 steps in memory formation:

1) A series of events are encoded by the hippocampus, and a reference is made to their memory location – hippocampal index (File Allocation Table)
* There is a mixture of Smell (S), Visual (V) and Auditory (A) signals that combine to give a memory
* These sensations all go to the somatosensory cortex and are all also pushed out to different areas of the brain cortex where the sensory information came in and processed
* E.g sensory input from the eyes goes to the occipital lobe and is processed in the parietal lobe
* Smell goes to the olfactory cortex and is processes by association cortices throughout the hemispheres

2) If this information is recalled prior to consolidation, the hippocampus performs the retrieval from its index of the events
* There are a bunch of disconnected activated cells across the cortex, when stimulated together, will give the same memory

3) After consolidation of the memory, retrieval can be initiated directly from the sensory cortices
* With repeat access, these sets of memory triggers become connected to each other, and exist on the cortex alone

18
Q

What is plasticity in LTM?

What is this method being used for?

A
  • Long-term synaptic plasticity is defined by a long-lasting, activity-dependent change in synaptic efficacy.
  • Plasticity in LTM is being researched forcounselling for post-traumatic stress disorder
  • patients are asked to re-live the events leading to PTSD then given an adrenergic beta receptor blocker (propranolol) which blocks re-consolidation of the memory
19
Q

Where does consolidation of declarative memory take place?

What is consolidation a result of?

A
  • Consolidation of declarative memory take place in the medial temporal lobes
  • Consolidation is a result of physical changes at the synapse
20
Q

What changes is LTM associated with?

Describe the 4 changes in morphology on dendritic spines that have been associated with LTP

A
  • LTM memory (consolidation) is associated with changes in connectivity (synapses) in networks of neurons predominantly in the cortex
  • 4 changes in morphology on dendritic spines that have been associated with LTP:

1) Synapses may increase in number of presynaptic vesicles (more neurotransmitter), posy-synaptic receptors and ribosomes (red circles)

2) Synapses may develop separate synaptic zones divided by a wall or a cleft (perforated synapses) in the spine

3) A single spine may divide into

4) New dendritic spines (white arrows) appear approximately 1 hour after a stimulus that induces LTP

21
Q

Consolidating Non-declarative memory & the striatum.

Label the Structures labelled involved in non-declarative memory (in picture)

A
22
Q

What does the corpus striatum consist of?

What is its role in consolidating non-declarative memory?

What functions does the cerebellum influence?

A
  • Corpus striatum (part of Basal ganglia) = caudate nucleus + putamen
  • It is thought to influence memories involving movement & procedural memory e.g. Olympic diving
  • The cerebellum influences fine motor learning including speech movements
23
Q

Describe the following types of amnesia:
1) Dissociated amnesia
2) Retrograde amnesia
3) Anterograde amnesia

How can the degrees of retrograde amnesia and anterograde amnesia vary?

What does this support?

A
  • Amnesia occurring without any other deficits is known as dissociated amnesia
  • Retrograde amnesia is a form of memory loss that causes an inability to remember events from the past
  • Anterograde amnesia is a type of memory loss that occurs when you can’t form new memories.
  • In the most extreme cases, this means you permanently lose the ability to learn or retain any new information
  • The relative degrees of retrograde and anterograde amnesia can vary, so supporting the view that storage and retrieval of memories involve different processes
24
Q

Pathology of memory. Describe the case of HM

A
  • Pathology of memory
  • The case of HM:
  • Patient HM suffered from severe epileptic seizures from aged 9 following a bike accident
  • These increased in severity with time until he was getting up to 10 minor seizures per day, and a major one every few days.
  • The source was assumed to be the medial temporal lobes At age 27 (1953) he was operated on by William Scoville and had an 8 cm length of medial temporal lobe removed bilaterally (which included entorhinal cortex, amygdala and the anterior 2/3 of the hippocampus)
  • The surgery alleviated his symptoms and there was no effect on perception, intelligence (reportedly improved) or personality (some loss of smell) his working memory however is normal
  • His memory loss took the form of profound amnesia of two forms

1) He had some retrograde amnesia in that he had no recollection of some years before his operation

2) He had extreme anterograde amnesia characterised by:

a) an inability to remember the identity of people he had just met and

b) an inability to remember numbers or events - e.g. his own age (constantly surprised) or the death of his mother

  • The specificity of his losses make the HM case a valuable model in the study of memory and he has been investigated by over 100 research teams
  • So with HM the memory of distant events was conserved.
  • His problem was therefore, an inability to consolidate new declarative long term memories
  • He learned some facts (President of the USA) but never recognised his psychiatrist Brenda Milner
  • Interestingly his anterograde memory deficit was uniform across all declarative modalities (visual, auditory, or other), but his short term working memory was intact.
25
Q

Was the ability to form non-declarative memories impaired in HM?

What does HMs case illustrate?

A
  • Was the ability to form non-declarative memories impaired?
  • He was able to learn to learn and retain how to draw in a mirror – viewed as a skill and therefore non-declarative
  • HM’s case illustrates that declarative, non-declarative, short term and long-term memory are not processed in the same place or by the same mechanisms
26
Q

Diencephalon and amnesia.

Describe the case of patient NA.

A
  • Diencephalon and amnesia.
  • The case of patient NA:
  • Aged 21, whilst in the armed forces a colleague accidently thrust a miniature fencing foil up through NA’s nose and into the left dorsomedial thalamic nucleus.
  • In addition, his Mammillary bodies were damaged bilaterally.
  • The hippocampus however was undamaged Diencephalon and amnesia In this patient cognition was normal and his IQ was unaffected (125). He suffered from some retrograde amnesia extending about 2 years prior to the accident but also profound anterograde amnesia
27
Q

What idea do the cases of HM and NA support?

A
  • Taken together with the case of HM this supports the idea of a functional link between the dorsomedial thalamus and the medial temporal lobe (hippocampus and associated structures) in memory consolidation