Lecture 7 Flashcards

1
Q

Define learning

A

A behavioural experience associated with change that allows some form of adaptation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define memory

A

The encoding of the learning experience that involves a physical change in the brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is associative learning?

A

Learning that is based on associations between different phenomena. For example, classical conditioning like Pavlov or operant conditioning.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is non-associative learning?

A

Learning that isn’t based on associations, for example habituation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the function of learning?

A

It has an adaptive advantage, it allows organisms to respond to the environment and it allows them to develop efficient responses to negative and positive stimuli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Discuss Karl Lashley’s work

And Thompson’s

A

He built on the idea of classical conditioning (strengthened connections between two areas of the brain). From this, he created the term Engram which is where memories are stored. He tried to find where memories are stored by making lesions in the brain to find the connections between the conditioned and unconditioned stimuli. The cuts (in a rat’s brain) didn’t impair learning, except if there were multiple large lesions. He concluded that there’s equipotentiality (all parts of the cortex contribute equally to complex behaviours) and mass action (the cortex works as a whole). However, Thompson found increased responses/changes in the lateral interpositus nucleus during learning, which is in the cerebellum. When this area (LIP) was suppressed, learning didn’t occur. The red nucleus in the midbrain receives input from the cerebellum and is crucial for the performance of a conditioned response but not for learning. Although, it’s not good to focus on a specific area as many areas will be involved.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Discuss Hebb’s work on memory

A

Hebb believed that there are two different processes. The process for short term and long term memory. Short term has limited capacity and the memory is lost after a few seconds. Long term has unlimited capacity and hints help you reconstruct the memory. Both types of memory work better when there’s meaningful context, this is consolidation. They then explored another type of memory which is located between short and long term memory, it’s called working memory. Working memory stores information still in use that’s still relevant. This information is crucial for cognitive activities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What area of the brain is involved in working memory?

A

This is tested via delayed response tasks where participants are tested about stimuli they saw a short while ago. They record the brain activity during the delay. It was found to be involved with the pre-frontal cortex but there are still issues between structuralists and functionists.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the opposite of habituation?

Habituation is an ancestral form of learning.

A

Sensitisation; increased responses to unpleasant stimuli after a shock. This can happen because of changes in synaptic activity, allowing the behavioural plasticity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Discuss the Hebbian synapse theory

A

When there is simultaneous activity in the pre and post synaptic neurons, which increase the effectiveness of each action potential. So if an axon stimulates a cell that has recently been stimulated, the response is increased. It basically becomes more efficient at activating the neuron. A long term potentiation is when an axon repeatedly stimulates dendrites/synapses which makes them more responsive for a period of time. A long term depression is when axons aren’t activated repeatedly and therefore become less responsive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Discuss the hippocampus and amnesia

Give a case study

A

When people get amnesia, we can explore the area of the brain that is damaged to see its effect on memory. For example, one patient (H.M.) had severe epilepsy, they had a bilateral ablation of the hippocampus. This reduced the seizures but impaired memory severely. His working memory and language remained intact, however, he couldn’t form long-term memories. He had procedural memory (motor skills and responses) but not declarative memory (describing memories). There are two types of declarative memory; semantic (specific facts) and episodic (personal experiences/memories). He also had implicit memory (recent experience influencing behaviour) but poor explicit memory (impaired ability to recall information). Therefore the hippocampus is important for new memories and declarative, explicit memories but not important for old memories and procedural, implicit memories. However, in this study, other areas as well as the hippocampus were removed (the temporal cortex).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the two types of amnesia?

A

Anterograde amnesia; memory loss of events that occur after brain damage.
Retrograde amnesia; memory loss of events that occurred a few years before brain damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the three main hypotheses about the role of the hippocampus?

A

It’s specialised for declarative memories (Patient H.M.).
It’s specialised for spatial memory (Maguire et al./Healy et al.).
It’s specialised for configural learning (remembering stimuli relative to other stimuli, for example, matching similar shapes or associating smoke with crackling sounds, it binds the information together).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Korsakoff’s syndrome?

What is Alzheimer’s disease?

A

It’s a type of brain damage that leads to amnesia. It’s found mainly with alcoholics caused by a thiamin deficiency which metabolises glucose (brain fuel). This causes neurons to shrink in the brain; mamillary bodies of the hypothalamus, parts of the hippocampus and the dorsomedial thalamus. This causes confusion, both types of amnesia, an effect on working memory. People try to fill in the gaps aka confabulations and they would usually guess but actually recall true memories. This disease is more prefrontal than Alzheimer’s allowing the confabulations.
This is caused by an accumulation of a protein called amyloid. The protein causes widespread atrophy aka wasting away, of the cerebral cortex and other areas. The hippocampus wastes away causing a loss of consolidation and binding and the cortex wastes away causing a loss of executive control and storage. It’s associated with ageing. Memory gets worse but they are better at implicit and declarative memory although it’s still impaired. It’s genetically related to Downs syndrome, however half of all cases aren’t related to genetics so there could be environmental effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly