Memory Flashcards
What is Hebbian learning?
When an axon of cell A excites cell B and repeatedly or persistently takes part in firing it, A’s efficiency, as one of the cells firing B, is increased
–> Neurons that fire together, wire together
Does LTP have anything to do with memory?
Suggested synaptic strength might be enhanced by concurrent activation in pre- and post-synaptic neurons
Exactly what occurs in LTP
What are the main measures of the Morris water maze?
- Escape latency
- Spatial transfer test
How do we know the hippocampus is involved in memory regarding the Morris water maze?
Both of the main measures (escape latency, spatial transfer test) are disrupted by hippocampal lesions
Explain the study by Morris (1989)
3 days of training 8x2 min trials per day
Animal removed if failed to find platform in 2 min
Received bilateral injection of NMDA antagonist into hippocampus; two doses - low and high
High dose significantly lengthened escape latency
Low dose - no effect
Examined effect of same doses on hippocampal LTP
High dose almost completely blocked LTP
Low dose - no effect
Explain study by Wilson and Tonegawa (1997)
Used knockout mice CaMKII
W + T produced mice lacking a critical subunit of the NMDA receptor in CA1 cells of hippocampus
Tetanic stimulation of Schaffer collateral –> CA1 synapses failed to induce LTP
Tested animals in Morris Water Maze
NMDAR 1 knockout mice did not focus on trained location suggesting that they had not learnt or remembered where the correct quadrant was
Describe the study by Castro et al. (1989)
Rationale = induction of LTP prior to learning should disrupt learning
Effect of inducing LTP in dentate gyrus on performance in Morris Water Maze
3 groups = control + 2 tetanised groups
Low frequency stimulation of perforant pathway each day to measure EPSP in dentate gyrus
After 5 days of baseline, tetanised groups received: repeated tetanic stimulation of perforant pathway 1/day for 14 days
In the period where the tetanised group received tetanic stimulation, the fractional change increases over time meaning the intensity of LTP got gradually got stronger across the days
Following the stimulation period, the fractional change decreased again
Tested escape latency on day 19 - little evidence of learning in tetanised group
Tested again on day 34 after decay of LTP and escape latency had decreased showing the animals had the ability to learn again
What evidence is there against a link between hippocampal LTP and memory?
Abeliovich et al. (1993)
More knockout mice this time lacking protein kinase C (enzyme that alters proteins)
Looked at the effect on LTP and learning
Mice lacking protein kinase C failed to show LTP
Unimpaired in Morris Water maze
9 days of training
No significant difference between ‘wildtype’ and knockout animals in escape latency
–> Blocking LTP did not affect escape latency or learning
Can LTP elsewhere be linked to memory?
Another structure involved in learning = amygdalar complex
How is the amygdala involved in pavlovian conditioning?
US –> UR (food –> salivation)
CS + US –> UR (food + bell –> salivation
CS –> CR (bell –> salivation)
Learning the association between US (food) and CS (tone) = establishing a simple ‘memory’
According to Pavlov (1927):
Conditioning requires changes in the pathway that mediates the CS, due to convergence of inputs from US
What did Rogan et al. (1997) study?
Conditioned fear response
US –> UR (foot shock –> fear response - ‘freezing’)
CS + US –> UR (foot shock + tone –> freezing
CS –> CR (tone –> freezing)
Conditioned fear involves the amygdalar complex
Explain what happens during conditioned fear and LTP
A tone (CS) evokes a field potential in the amygdala; early part (the ‘dip’) reflects activity in a pathway bringing auditory information from the thalamus
During training, CS and US are paired (US just after CS)
After training, CS produces larger amplitude ‘dip’ in field potential; CS also produces freezing
Important: repeated presentation of CS (tone) alone leads to ‘extinction’ of freezing response, and reduction in size of dip
What did Schroeder and Shinnick-Gallagher (2005) find in relation to amygdala LTP?
Conditioned fear
CS = white noise tone
US = foot shock
Paired ten times a day for 2 days (fear-conditioned group)
Unpaired controls (UP) received same number of CS and US presentations in psuedorandom fashion
Stimulated pathway from cortex to amygdala
EPSPs were measured in naive control and unpaired and fear-conditioned animals 1 day and 10 days post-testing
In the feared condition group the field potential was bigger at every point in the slope
What is an alternative hypothesis for LTP?
Shors and Matzel (1997)
LTP = an arousal or attention ‘device’
Basic function is to increase impact or gain of salient environmental stimuli
Salient = novel and/or fear provoking
Propose that these stimuli produce LTP-like changes in the brain which increases attention to them
Increase in impact may facilitate learning indirectly
