Memory Flashcards
What is Donald Hebb’s proposal for associative learning?
When axon of cell A excites cell B and repeatedly/persistently takes part in firing it, A’s efficiency, as one of the cells firing B, is increased - cells that fire together, wire together
Synaptic strength might be enhanced by concurrent activation in pre- and post-synaptic neurons
LTP is this exact phenomenon
What is the Morris water maze?
Tests for spatial memory
Opaque liquid ie milk (great, torture animals in the products of animal torture - 10/10 neuroscience), submerged escape platform, over sequential submersions rats to learn location of platform based off cues in the room
Measures:
Escape latency - how long to get out over time
Spatial transfer test - remove platform, see where stays most
- both of these are disrupted by hippocampal lesions..
What did Morris 1989 study?
NDMA antagonists
Morris water maze
3x days training, 8x2mins/day
Before training: two groups had bilateral injections of NMDA antagonist (negatively impacts LTP) into dentate gyrus in hippocampus - one high/one low; one control group
High dose = longer escape latency on at 3 + blocked LTP; low dose = nil effect
What did Wilson and Tonegawa 1997 study? (Knockout mice)
NMDAR1 receptor knockout mice in CA1 neurons only = non-functional
Tetanic stimulation of Schaffer colatteral - CA1 synapses failed to induce LTP
Placed in Morris water maze - no evidence for learning
(correlational evidence)
What did Castro et al 1989 study?
Prior LTP
Induction of LTP prior to learning should disrupt learning
3 groups - one control + 2 tetanised: measured EPSPs using test tetanised pulses at baseline for 5 days before being tetanised
This induced LTP in dentate gyrus and looked at Morris water maze performance at peak EPSP level (most saturated synapses, potentiation peak) at day 19 - no improvement in escape latency in tetansied group
Tested again after decay of LTP - found control levels of escape latency
(more causative)
What did
Albeliovich et al 1993 study?
(Protein kinase C)
An example of contrasting results
Protein kinase C knockouts - failed to show LTP in hippocampus but unimpairment in Morris water maze
Why is there a difference in the findings of studies concerning LTP and spatial memory?
Not enough is known about hippocampal role in it - combination of memory + proprioception = complex - how do we manipulate properly?
Maybe no relationship between the two… (unlikely)
What is the role of the amygdala in memory?
Classical conditioning = formation of a very simple memory:
US->UR; CS + US -> UR; CS -> CR
May also involve LTP processes..
What did Rogan et al 1997 study?
Conditioned fear
Foot shock -> freeze can be conditioned to a tone
Tone evokes a field potential in amygdala - early ‘dip’ = thalamo-amygdala auditory information transfer
Conditioned tone to be associated with foot shock - when fear response learned = larger ‘dip’ ; when repeated presentation of tone alone = extinction of fear response + decrease in size of dip
What did Schroeder and Shinnick-Gallagher 2005 study?
LTP and long term fear
Conditioned fear to white noise
Fear response in amygdala tightly controlled by frontal cortex - frontal lesions = cant learn fear; lesion once learned = cant extinguish response
Fear related EPSPs still greater 10 days after pairing
What is an alternative hypothesis for the role of LTP in memory?
Shors and Matzel 1997
LTP = arousal/attention device - increasing the gain of salient environmental stimuli = indirect impact on learning
No positive evidence but may explain negative findings?
Need to ensure we’re not seduced by superficial appeal of the relationship
