Lec 11- Learning and memory Flashcards
1
Q
definition of learning and memory
A
- Learning- acquisition of new information or knowledge
- Memory- the retention of learned information
2
Q
Human memory- Declarative
A
- Daily episodes
- Words and meanings
- History
3
Q
Human memory => Procedural
A
- Motor skills
- Associations
- Priming cues
- Puzzle solving
4
Q
The temporal lobes and declarative memory
A
- Electrical stimulation => Temporal lobes => Hallucinations recollection of past experience
- Ablation => Temporal lobes => Retrograde or anterograde amnesia impairment of long term memory
5
Q
HM and Temporal Lobectomy
A
- Anticonvulsant resistant seizures
- Bilateral removal of medial temporal lobe was successful in alleviating seizures
- No effect on personality, intelligence or perception
- Extreme anterograde amnesia- lacks the ability to form new declarative memories
- Procedural short term and long term memory was normal
6
Q
Henry Gustav Molaison
A
7
Q
Normal v H.M.
A
8
Q
Hebb and memory storage
A
- Activity will occur (external stimulus) and activate a certain amount of cells within the hippocampus
- Paramydal cells will fire in a certain pattern
- The more times this stimulus occurs then more cells will fire
- After time even if we get a part of a stimulus we can still identify the stimulus as a whole
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9
Q
Hebbs law
A
- Donald Hebb (1949) a Canadian scientist, said that when 2 neurones are active
- so that one repeatedly releases neurotransmitter at the same time as its post-synaptic partner is firing APs
- Then that synapse will become stronger
- This is call Associativity
- It is sometimes said that ‘cells that fire together wire together’
10
Q
The neural basis of memory
A
- Changes in neuronal wiring and synaptic connectivity in response to external stimuli- the stronger the connection the greater the chance of cells firing together
- Modification in the efficacy of synaptic transmission- synaptic plasticity
- Triggered by neural activity and production of second messengers
- Can result from alterations in existing synaptic proteins
11
Q
A
- We need both the somatosensory system and auditory system to both converge on another neurone to produce a memory
12
Q
The hippocampus
A
- Rats hippocampus takes up a large portion of brain so there capacity for learning is relativly high
- All soma of the neurones line up, all axons from cortex synapse into dendrites
13
Q
An increase in the strength of a synapse after strong stimulation is called Long Term Potentiation (LTP)
A
- Titianic stimulus (lots of stimulus in a short amount of time)
- Or many synapses converging at once to give a large stimulation (EPSP)
- Both of these cause Long-Term Potentiation (LTP)- raising the strength of the synapse for a long time such as for life
14
Q
So why does the EPSP become larger
A
- Increased excitability of post-synaptic cells- t
- Increased number of AMPARs
- Increase glutamate release- NMDAR stimulation
- Formation of new synapses
- Dependent on age- lose the ability to form memory by some pathways
- All of these- depending on circumstances
15
Q
Properties of NMDAR LTP (Long-term potentiation)
A
- LTP is synapse-specific- Activity between 2 cells may only occur at one synapse
- It is induced by NMDAR activation
- It is expressed by AMPAR (the bigger EPSP)
- It is maintained by changes in the number of post-synaptic AMPAR and structural changes (proteins)
17
Q
LTP INDUCTION has a threshold
A
- There is a threshold for the establishment of long-term potentiation
- The low rate of stimulation does not depolarize membrane sufficiently- low-level activity can actively reduce the strength of the synapse
- EPSP produced by a high rate of stimulation summate and reach the threshold
18
Q
LTP is blocking by NMDAR antagonist and by removing Ca2+
A
- Ketamine, Phencyclidine (PCP)
20
Q
LTP maintenance- AMPAR insertion
A
- NMDAR opens
- Ca ion enters and activates CAMK-II
- Linking proteins attach to CAMK-II- Scaffolding proteins pull vesicles to the surface
- AMPAR delivered to the membrane in vesicles
- Additional AMPA receptors inserted in the membrane
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21
Q
AMPAR insertion- ‘silent’ synapses
A
- Initially, synapses may have the only NMDAR
- If there is sufficient depolarization from a neighbouring synapse, they may become ‘Unsilenced’ and AMPARs inserted into the membrane
- Only NMDAR means no matter how much glutamate occurs there is no stimulation = NO depolarisation (AMPA needs to act first to depolarise to allow NMDAR to activate)
- If we have enough depolarisation at neighbouring synapses that can be enough to shift Mg from NMDAR and AMPA receptors will be inserted hence that synapse can now be depolarised
22
Q
A
- Very active dendritic spines can multiply (lumps on dendrites that form post-synapse)
- Spines are the physical correlate of memory
- Not enough activity can cause spines to die (this is why we have to constantly revise for exams because as activity of this synapse decreases it dies)
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23
Q
The Morris Water Maze
A
- Before training- the path is long, slow and random
- After training- the path is short and direct- grid cells fire in a particular way (synchronize) to map out the maze or path
- Role of place cells- O’Keefe UCL Noble Prize Physiology 2014
- Lesion of hipposampus or AP5
- The training has no effect, path is long, slow, random
25
Q
The reverse process-LTD
A
- Long-term depression
- Also NMDAR dependent
- Non-coincident activity reduces EPSP size
- Synapses constantly under pressure to get stronger or weaker
- This forcing of synapses to reduce there activity EPSP without constant activation (so reduce memory) is known as homeostatic plasticity
