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Learning & Memory
Biological Psychology, PPP-2013, Bangor University
Terms in this set (32)
What is the point in learning and memory? 1st point
Important with regard to survival- so our learning and memory systems are complex due to evolutionary necessity for detecting/avoiding threat
What is the point in learning and memory? 2nd point
Important in regard to understanding how individuals are shaped by prior experiences to respond the way they do- changes the way we respond in future situation
What is the point in learning and memory? 3rd point
Important in understanding when it goes wrong, such as Alzheimer's. Also when it's 'too good', such as PTSD (memories are too strong and easily retrieved)
Define Learning and Memory is biological terms
The acquisition and retention of changes in behaviour
Define Synaptic Plasticity
The ability of synapses to strengthen/weaken over time, in response to increases/decreases in their activity
If a synapse repeatedly becomes active about the same time as the post-synaptic neuron fires, then either the structure/chemistry of the synapse will changer in a way that strengthens it
Evidence for Hebb rule
1970's by Lomo and Bliss, who found that if they applied a burst of 100 electrical pulses over a couple of seconds to one of the pathways leading to the hippocampal formation, then a single pulse applied later would show an increased response in the structure at the end of the pathway, within the hippocampal formation- This is called Long-term Potentiation
Long-term potentiation (LTP)
The activity that leads to LTP is determined by how strong the activity at the synapse. The occurrence of LTP will be determined by the release of glutamate and its action on AMPA and NMDA receptors. If NMDA receptors are active pre/post synaptically, then calcium will enter the postsynaptic neuron and this will effect LTP.
Long-Term Depression (LTD)
The removal of AMPA receptors- results in a decreased efficiency of the synapse. Opposite of LTP and thought to occur due to memory decay within the hippocampus/ motor learning within the cerebellum
Pathways in the brain that support LTP and LTD
Several pathways in the brain support both LTP and LTD, including those in the amygdala, the association cortices and the prefrontal cortex
Major form of learning- involves learning to recognise new stimuli or involve learning to recognise changes/variations within known stimuli- often unaware of this type of learning, as it happens outside of conscious awareness
Why does visual recognition take place?
Due to changes in synaptic connections in the visual association cortex (which is in the Occipital Lobe) that establish new neural circuits; when the same item is seen again, these circuits become active, leading to recognition.
Evidence of Perceptual learning
Penfield and Pert- stimulating visual association cortex lead to memories of images
A focus on conditioned emotional responses (Think of Little Albert) Unconditioned stimulus leads to unconditioned response. After repeated pairings, conditioned stimulus leads to conditioned response. Gong = crying. Fluffy rat is paired with gong = crying. Now whenever fluffy rat is placed in front of Albert, he will cry without the gong being hit, as he has conditioned the noise of the gong with the fluffy rat.
Operant Conditioning / Instrumental Conditioning
Means through which we profit from experience. If we make a response (action) that has a favourable outcome, then we are more likely to make that response again- our response is reinforced. Tesco clubcard- shop at tescos, collect points, able to spend them later on
Circuits involved in instrumental conditioning
Begin in various areas of sensory association cortex of frontal lobe.
Two major pathways- 1.) Transcortical pathways between sensory and motor association cortices and 2.) Basal ganglia and thalamic pathways
While learning to drive, these pathways will be involved in getting hold of complex behaviours relevant to deliberation and instruction.
Basal ganglia and thalamic pathways
Overtime, these actions become rehearsed and habit like, so the basal ganglia and thalamus take over this process. They were passive observers learning what we do before they take over. As actions become learned and we don't need to think about them, then the basal ganglia takes over, freeing up the transcortical circuit to learn new things
How are we incentivised to repeatedly make the same actions if they lead to favourable outcomes?
There are several reinforcement mechanisms in the brain, but the activity of dopamine neurons is especially important (mesolimbic/mesocortical dopaminergic systems are central to this)
The action of reinforcement
Mesolimbic dopamine system begins in the ventral tegmental area (VTA). Projects to forebrain, amygdala, hippocampus and nucleus accumbens (NAC). Neurons in the NAcc project to the ventral part of the basal ganglia. Mesocortical dopamine system also begins in VTA and projects to prefrontal cortex, limbic cortex and hippocampus.
The action of reinforcement (Part 2)
The medial fore-brain bundle connects the ventral tegmental area to the nucleus accumbens. If the medial fore-brain bundle or the VTA is stimulated by reward, then dopamine is released from the nucleus accumbens.
E.g The neural circuits in the VAC that recognise someones face are connected to circuits in many other parts of the brain, and these are connected to many others. Includes the establishment and retrieval of memories of events, episodes and places.
The inability to learn new information. Can remember events that occurred in the past but cannot remember information encountered after the brain damage- rare, often occurs with at least some retrograde amnesia
Inability to remember events that happened before the brain damage occured
Destruction of the mammillary bodies often due to chronic alcoholism
Anterograde amnesia causes- Damage to the temporal lobes
Cases from patients who had temporal lobe surgery in order to relieve seizures resulting from epilepsy-
Classic case is H.M
Closer examination of patients like H.M
Originally thought that they were unable to convert STMs into LTMs. However, it seemed that perceptual learning, classical conditioning and motor learning were still intact and thus a total failure in new learning is not an accurate description of anterograde amnesia
Anterograde amnesia causes- Hippocampus
Damage to the hippocampus or to the regions that supply its inputs and outputs can cause AA.
Memories that are 'explicitly available to conscious recollection as facts, events or stimuli' (Squire, Shimamura and Amaral, 1989)
Memory for events that we can think and talk about- explicit memory
Memories that we are not necessarily conscious of. Implicit memory- we don not need to think about the actions as we perform them
Recieves info from sensory/motor association cortex and from basal ganglia and amygdala. It processes this information and modifies memories by linking them together and allowing us to remember relationships between the relevant events.
Hippocampus, in relation to declarative/non-declarative memories
Hippocampal formation transforms declarative memories into permanent storage- before complete, HF is needed to retrieve these memories. Once transformation has taken place, the hippocampal formation is not needed to retrieve these memories. Explains why people with AA will retain memory for evens long before injury. Also explains why new declarative memories are unable to be formed at all, as well as why there might be some deficit for memory (retrograde amnesia) in the time leading up to the injury.
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