W11 - Learning and Memory Flashcards

1
Q

What are the different types of memory?

A

Types of Memory
*Learning: acquisition of new information
*Memory: retention of learned information
*Declarative memory (explicit)
* Facts and events – hippocampus
*Nondeclarative memory (implicit)
* Procedural memory—motor skills, habits - striatum

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2
Q

What is Declarative and Nondeclarative Memory?

A

Declarative memory:
Medial temporal lobe; diencephalon
- Facts, events

Nondeclarative memory:
*Procedural memory: skills and habits (Striatum)
*Classical conditioning:

-Skeletal musculature (cerebellum)
Eg. dog will salivate when presented with food. Can ring a bell whenever it is given food. Eventually, when the bell rings without food, the dog will salivate due to the conditioning.

-Emotional responses (Amygdala)
Eg. Fear of snakes from reading, watching TV etc.

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3
Q

What are the Types of Declarative Memory?

A

*Working memory
* Temporary storage, lasting seconds
*Short-term memories—vulnerable to disruption
* Facts and events stored in short-term memory
* Subset are converted to long-term memories.
*Long-term memories
* Recalled months or years later

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4
Q

What is memory consolidation?

A

Memory consolidation: process of converting short- to long-term memories

Sensory information gets converted to Working memory or STM. STM gets consolidated over time and enters Long-term memory.

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5
Q

What is the Prefrontal Cortex linked to?

A

Prefrontal Cortex is linked to Working Memory
*Primates have a large frontal lobe.
*Functions of prefrontal cortex: self-awareness, capacity for planning and problem solving

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6
Q

How do we know the working memory resides in the pre-frontal cortex?

A

Working Memory Activity in Monkey Prefrontal Cortex: delayed response task

A monkey is sat down infront of a desk with two wells in it. A food reward is placed in one of the wells and the monkey sees it. A screen will come down between them for a finite amount of time - delayed time. The wells will then be covered over and the screen is retracted. Then there is a choice period, where the monkey can choose one of the wells and retrieve the food reward.

Electrical activity of the brain is recorded during this period of time. Slightly elevated activity in the “cue period”, where monkey sees the food being placed in the well and the “choice period”.

The highest level of activity is in the delay period where the monkey is retaining the information - working memory.

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7
Q

In the monkey retaining information about where the target is flashed onto the screen, what other brain regions are involved?

A

Other brain regions are involved, for example lateral intraparietal cortex neuron response in delayed-saccade task

Experiment:
Animal is trained to look at a fixation point on the screen. While it is looking, a target is flashed onto the screen briefly and there is a delay where the animal keeps looking at the fixation point. Through food rewards, the animal is then trained to look at the place the flash took place. The rapid eye movement is then saccadic eye movement.

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8
Q

Where are memories stored though?

A

The engram - groups of memories that store neurones.

Hebb’s Cell Assembly and Memory Storage
- States that neurones exist in a network with reciprocal connections between them.
1) Activation of cell assembly by stimulus
2)Reverberating activity continues activation after stimulus is removed
3)Hebbian modification strengthens reciprocal connection between neurones simultaneously active.
4) Strengthened connections contain the engram for stimulus
5) After learning, partial activation of assembly leads to activation of entire representation of stimulus.

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9
Q

How does consolidation occur?

A

Consolidation: involvement of the medial temporal lobes
Hippocampus is located in the temporal lobe.
Rhinal sulcus, Perirhinal cortex and Parahippocampal cortex are regions that feed into the hippocampus.

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10
Q

How does Information flow through the medial
temporal lobe?

A

1) Sensory info
2) Cortical association areas
3) Rhinal and Parahippocampal cortical areas
4) Hippocampus -> 2)
5) Through fornix, Thalamus, hypothalamus - can pass info to other regions of the brain. This means the hippocampus doesn’t get full throughout life times.

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11
Q

What is amnesia? What are the types?

A

Amnesia: serious loss of memory and/or ability to learn.

Causes: concussion, chronic alcoholism, encephalitis, brain tumor, stroke

Reterograde amnesia:
Goes backwards, where consolidated memories cannot be received - loss of past memories.

Anterograde amnesia:
The memories of events until the event of trauma can be retrieved. Cannot form new memories.

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12
Q

What is the Henry Gustav Molaison study?

A

known as HM to neuroscientists)
Feb 26, 1926 - Dec 2 2008
* Had a bicycle accident at the age 9.
* Developed epilepsy (had seizures)
* In 1953 was referred to William Scoville
at Hartford Hospital.
* Scoville localised the epilepsy to the
right and left medial temporal lobes (MTL)
of HM’s brain and removed parts of the
right and left MTLs.
* The surgery was effective in reducing
occurrence of seizures. However, it had a
devastating side effect -
* HM lost the ability to form new long-
term memories but remembered events
before the surgery. He was, however, able
to learn new motor skills (although he
didn’t remember learning them).

Shows the hippocampus was central to memory consolidation. The memories he can retrieve maybe due to the hippocampus distributing the memories to other parts of his brain.

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13
Q

What was the impact of HM on memory research?

A

In 1957, Brenda Milner reported the profound effect on memory of bilateral medial
temporal lobe resection, carried out to relieve epilepsy in a patient who became known as
H.M. (1926–2008) (Scoville & Milner 1957, Squire 2009) (Figure 1). Remarkably, H.M.
exhibited profound forgetfulness but in the absence of any general intellectual loss or
perceptual disorders. He could not form new memories (anterograde amnesia) and also
could not access some memories acquired before his surgery (retrograde amnesia). His
impairment extended to both verbal and non-verbal material, and it involved information
acquired through all sensory modalities. These findings established the fundamental
principle that memory is a distinct cerebral function, separable from other perceptual and
cognitive abilities, and also identified the medial aspect of the temporal lobe as important
for memory. The early descriptions of H.M. can be said to have inaugurated the modern era
of memory research, and the findings from H.M. enormously influenced the direction of
subsequent work.”
From “The Cognitive Neuroscience of Human Memory Since H.M
By Larry R. Squire and John T. Wixted
Annu Rev Neurosci. 2011; 34: 259–288.
This review highlights studies on other patients that pinpointed the hippocampus as critical
for memory.

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14
Q

What is the case of Clive Wearing?

A

He was a very talented musician - involved in music for Charles and Diana’s wedding.
Viral encephalitis - inflamed parts damaged hippocampus. Devastating effects on both retrograde and anterograde declarative memory.
He lives in a loop where he is constantly living in the present.

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15
Q

How do you test spacial memory?

A

Place Cells and special memory.
* Learning Morris water maze requires hippocampus.
* Place cells fire when animal is in a specific place.
* Place fields dynamic

Experiment:
A large wadling pool is filled with water and it is made opaque. There is a platform built into the pool, where the mouse would be able to stand on and get out. In the maze, it swims around until it finds the platform and gets out. If you repeat this a few times, it should help with the navigation. The mouse would then swim straight to the platform. This type of learning is dependent on an intact hippocampus. If you disrupt the synaptic pathways, you can block this learning process.

Not all cells are created equally within the hippocampus. There are Place cells - these fire when the animal is in a specific place. When animals get habituated to certain places, these cells start firing.

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16
Q

What are the Two Models of Memory
Consolidation?

A
  • Standard model of memory consolidation
  • Information from neocortex areas associated with sensory systems sent to medial temporal lobe for processing
  • Synaptic consolidation, systems consolidation
  • Post consolidation, hippocampus not necessary
  • Multiple trace model of consolidation
  • Hippocampal involvement is continued - there is scope for consolidated memories to be tweaked.
  • Multiple memory traces
  • Dependent upon synaptic plasticity – ‘the biological process by which specific patterns of synaptic activity result in changes in synaptic strength’
17
Q

What is the model of distributed memory?

A

Rather than having one memory in one neurone, they are distributed to multiple neurones in the network.

18
Q

How are the changes in neuronal response made?

A

The changes in neuronal response can be explained by synaptic plasticity. The trisynaptic circuit of the hippocampus is often used in
studies of this phenomenon.

Trisynaptic circuit:
* Information flows from entorhinal
cortex, via performant path to the
dentate gyrus
* Mossy fibres originate from dentate
gyrus and synapse upon pyramidal
neurons in CA3 hippocampal region
* Axons from CA3 (Schaffer collaterals)
synapse upon pyramidal neurons in
CA1 hippocampal region

19
Q

What is the Bliss and Lomo (1973)Long-Term Potentiation (LTP) in CA1 region of the
hippocampus?

A

They had a hippocampal slice preparation and stimulated the Schaffer collaterals and recorded the CA1 neurones.
Depending on the frequency of stimulation, you get a change in the excitatory post synaptic potential (EPSP).
Low frequency = there wasn’t much difference
High frequency = magnitude in response to the EPSP, greatly increased.

If you continue to stimulate neurones that are very high frequency, you will get increased responsivity. Called LTP because it can be maintained for a significant period of time.

20
Q

What are the Mechanisms of LTP in CA?

A
  • Glutamate receptors mediate excitatory synaptic transmission.
  • NMDA receptors and AMPA receptors

Normally, Glutamate activates AMPA and NMDA receptors, and the gates will open letting Ca2+ flood in. If you stimulate the release of increased glutamate receptors, you get the significant activation of AMPA therefore NMDA receptors. Leads to a great rush of Ca2+ leading to activation of Calcium calmodulin kinases.
Effects:
1) Increase phosphorylation of AMPA receptors already in the membrane - increases responsivity - magnifies EPSP.
2) Increased expression of receptors in the post synaptic membrane.

  • More responsive receptors and a larger overall population of receptors = increase in post synaptic response.
21
Q

What are some structural changes following LTP?

A

Dendritic spine growth