NEURO: Learning and Memory Flashcards

1
Q

What is the difference between learning and memory?

A

LEARNING: acquisition of new information

MEMORY: retention of learned information

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2
Q

What are the different types of memory?

A

DECLARATIVE MEMORY (EXPLICIT): facts and events [hippocampus]

NON-DECLARATIVE MEMORY (IMPLICIT): procedural memory (motor skills, habits) [striatum]

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3
Q

What are the different types of declarative and non-declarative memory?

A

Declarative memory involves the medial temporal lobe and the diencephalon, and stores:

  • facts
  • events

Non-declarative memory stores:

  • procedural memory: skills and habits (involving the striatum)
  • classical conditioning in the skeletal musculature (involving the cerebellum)
  • classical conditioning in emotional responses (involving the amygdala)
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4
Q

What are the different types of declarative memory?

A

WORKING MEMORY:
- temporary storage, lasting seconds

SHORT-TERM MEMORIES:

  • vulnerable to disruption
  • facts and events stores in short-term memory
  • subset are converted to long-term memory

LONG-TERM MEMORIES:
- recalled months or years later

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5
Q

What is memory consolidation?

A

It is the process of converting short-term memories to long-term memories.
It involves the medial temporal lobes.

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6
Q

What part of the brain is involved in working memory?

A

The prefrontal cortex is involved with working memory.

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

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7
Q

How does the size of the prefrontal cortex affect working memory?

A

Because the prefrontal cortex is relatively large, it allows for greater capacity for higher-level thinking and bringing in working memory, allowing for:

  • self-awareness
  • capacity for planning
  • problem-solving
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8
Q

Where is memory stored?

A

Memory is stored in the engram, which is a collection of neurons that, when they act together, store a memory.

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9
Q

Which brain region is involved in memory consolidation?

A

medial temporal lobes

-hippocampus

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10
Q

Hebb’s cell assembly and memory storage

A

Presentation of an external stimulus resulted in the activation of a cell assembly, which is a group of interconnected neurones firing together

Collective firing causes reverberating electrical circuits within the neurones, continuing electrical activity even after the stimulus is removed

Causes Hebbian modification of circuits, resulting in strengthening of connections between the neurones that are active at the same time

The strengthened connections of the cell assembly contain the engram for the stimulus

After learning, only partial activation of the assembly leads to activation of the entire representation of the stimulus

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11
Q

Describe information flow through the medial temporal lobe.

A

We get sensory information coming in to our cortical association areas. This send the information through to the parahippocampal and rhinal cortical areas. This finally gets forwarded to the hippocampus.
Via the fornix, the information is sent to the thalamus and the hypothalamus. The hippocampus also relays back to the cortical association areas.

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12
Q

Hippocampus role in memory

A

involved in processing long-term memory:

  • closely associated with parts of the cerebral cortex (rhinal and parahippocampal cortical areas)
  • these structures run into the hippocampus and allow the funnelling in of neurones and information transmitted via those neurones into the hippocampus
  • once in the hippocampus, memories don’t necessarily stay there
  • they pass either through the fornix pathway to the thalamus and hypothalamus, or through pathways directly to other cortical areas
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13
Q

What is amnesia?

Causes of amnesia?

A

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

CAUSES: concussion, chronic alcoholism, encephalitis, brain tumour, stroke

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14
Q

Retrograde amnesia

Anterograde amnesia

A

Retrograde amnesia

  • problems recalling past events following trauma
  • still able to form new memories

Anterograde amnesia

  • past memory is unaffected
  • unable/severely limited in capacity to form new memories following trauma
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15
Q

Spatial memory

Which brain region is important for spatial memory?

What can disrupt spatial memory?

A

ability to navigate yourself safely around somewhere

hippocampus

lesioned hippocampus
pharmacologically blocking hippocampus

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16
Q

Place cells

A

neurones in the hippocampus that fire when the animal occupies a specific location within its environment
-can be used to process spatial information

17
Q

Studying spatial memory in animals

A

Morris water maze:

  • Large wading pool into which vast quantities of water poured into
  • Hidden platform located somewhere in the water
  • Rat placed in water, and its response would be to try and get out of the water
  • Rat will try and find the hidden platform to stand on it and get out of the water
  • After rat gets out of the water, there is a delay (few hours/day/week etc), then same rat is put into the water maze
  • If rats have retained the spatial information, they will just go straight to the hidden platform instead of swimming around and around
  • This is helped by other navigational cues in the pool and environment
18
Q

Models of memory consolidation

A

Standard Model of Memory Consolidation

Multiple Trace Model of Memory Consolidation

19
Q

Standard Model of Memory Consolidation

A
  • Information from neocortex areas associated with sensory systems sent to medial temporal lobe for processing
  • Synaptic consolidation, systems consolidation
  • Post consolidation where information has already gone through hippocampus and distributed around the brain (long term memories can be recalled without need for hippocampus)
20
Q

MULTIPLE TRACE MODEL OF CONSOLIDATION:

A
  • hippocampal involvement is continued

- there are multiple memory traces

21
Q

What are the models of memory consolidation dependent upon?

A

synaptic plasticity = the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity

22
Q

Describe the relationship between spatial memory and place cells.

A

Via animals learning the Morris water maze, we know that learning to do with spatial memory requires the hippocampus.
The place cells will fire when the animal is in a specific place. The place fields are dynamic.

23
Q

Describe the model of distributed memory.

A

particular memories are spread across neurones

It can also explain when, when we lose some neurons, we don’t necessarily lose all our memories associated with the neurons, as there are others with the information stored.

24
Q

Trisynaptic circuit of the hippocampus

A

The trisynaptic circuit is a neural circuit in the hippocampus, which is made up of:

  • dentate gyrus
  • pyramidal neurons in CA3 hippocampal region
  • pyramidal neurons in CA1 hippocampal region
25
Q

Flow of information in trisynaptic circuit

A

1) Information flows from the entorhinal cortex, via the performant path to the dentate gyrus
2) Mossy fibres originate from the dentate gyrus and synapse upon pyramidal neurones in the CA3 hippocampal region
3) Schaffer collateral axons from CA3 synapse upon pyramidal neurones in CA1 hippocampal region

26
Q

Long Term Potentiation

A

an increase in a synapse’s firing potential after brief, rapid stimulation. Believed to be a neural basis for learning and memory.

27
Q

What are structural changes following long term potentiation?

A

dendritic spine growth

28
Q

Bliss and Lomo (1973)

A

Glutamate receptors mediate excitatory synaptic transmission (AMPA [initially] and NMDA receptors).

Structural changes following LTP include dendritic growth. discovered LTP in the CA1 region of the hippocampus:

  • Stimulating input 1 repeatedly causes a great increase in excitatory postsynaptic potential (EPSP) in the target neurone for any given stimulus
  • Target neurone, therefore, become more responsive, and there is a strengthening in that connection
  • This strengthening is very specific, because if there is stimulation of input 2, but not repeatedly, there is no increase in excitatory postsynaptic potential (EPSP)
29
Q

Mechanisms of LTP in CA1

A

1) Glutamate released by pre-synaptic membrane
2) Glutamate binds post-synaptic AMPA receptors and there is Na+ influx via AMPA receptor channels causing depolarisation of post-synaptic membrane
3) Mg2+ block on NMDA receptors removed, allowing Ca2+ and Na+ influx via NMDA receptors channels
4) This can lead to receptor trafficking- new AMPA receptors can be made and inserted on the post-synaptic membrane
5) The extra AMPA receptors causes for more Na+ influx
6) Na+/Ca2+ influx then activates an enzyme called P-CamKinaseII which can phosphorylate and increase the ionic conductance of the receptors, meaning more Na+ and Ca2+ is entering the cell
7) This trafficking of receptors can underlie a process called Long-term Potentiation (LTP), which is a synaptic strengthening (due to the extra AMPA receptors inserted and extra ionic conductance, causing for stronger synapses)
8) This is an important process that underlies learning and memory