Lecture 6- How to Store Memory Flashcards
Why is Atkinson and Shiffrin’s (1971) multi-store model of memory insuffiecient?
Doesn’t explain how memory works at the neuronal level
What did Donald Hebb say in the Organisation of Behavior (1949) about memory?
- Each psychologically significant event, sensation, percept, expectation, memory or thought is the result of a particular pattern of activity in a group of interconnected neurons (cell assembly).
- Way ahead of his time
What is the believed difference between the short term memory for an event and long term memory at neuronal level?
- Short-term memory= ‘reverberating’ activity in networks of neurons (sustained firing/ activity in the network of neurons associated with the event)
- Long-term memory= stored by changing the strength of connections between neurons in a network (consolidation). Means the neurons in the loop don’t have to constantly fire but they have a greater likelihood of firing in that specific pattern (reactivation). This reactivated leads to the remembering/ reliving of the experience.
According to Hebb - what rules governed whether a
synaptic connection would strengthen or not?
-If have a weak input and strong input into the same dendrite and they both fire at same time then the weak connection will get stronger so now have two strong inputs.
What is Hebbian learning?
-The idea that if the pre-synaptic and post-synaptic cell fire at the same time then the connection between them is strengthen. This can be simplified to the saying that cells that fire together, wire together.
How does Hebbian learning allow for the association of inputs using fear and crabs as an example?
- First think of an axon with two inputs. An input coming from a pain receptor will be strong while an input from the visual system will naturally be weak.
- You walk down the beach and you step on a crab. The pain input and visual input of the crab fire at the same time. This leads to an increase in synapse strength of the weak input (cued by the visual stimulus of crab). Now there are two strong inputs into the axon and the result is fear.
- Now just seeing the crab will result in fear as the loop of neurons involving pain, the visual info of crab and the emotion of fear has been consolidated by increasing the synapse strength.
What is the strengthening of synapses via artificial stimulation called?
Long-Term Potentiation (LTP). Means the EPSPs will be greater (greater strength of firing).
How long does LTP last?
years
How does LTP have Hebbian properties?
- LTP strengthening is confined to the activated pathway (synapse)
- LTP can occur in a weak pathway if another input to the cell is activated strongly at the same time
What is the LTP induction mechanism?
-Glutamate acts on AMPA subtype receptor brings in sodium to depolarize cell
-In response to this the NMDA subtype receptor is blocked with magnesium to prevent anything passing through
-As the cell becomes more positive the magnesium ion is repelled unblocking the NMDA channel.
-This allows more glutamate to bind to AMPA subtype receptors further along and more sodium to come in. Calcium ion can also come through the unblocked NMDA channels.
-Calcium influx leads to LTP induction via downstream changes.
This leads to increases in available receptors and then changes in
protein synthesis that can induce long-term alterations in the
shape and strength of the synapse
As well as changes in synapse strength after LTP leading to greater (EPSPs) what other change at the synapse occurs?
-Change in receptor + synapse shape (which facilitates the strength changes)
How would you test that LTP has anything to do with memory?
- Show that blocking LTP prevents memory formation
- Show that reversal of LTP produces forgetting
- Show that learning leads to LTP-like changes
- Show that producing LTP creates false memories or masks existing memories
How do we show that blocking LTP prevents memory formation?
Look at the effect of different doses of the NMDA antagonist AP5 (block receptor channel) on LTP
What does the Morris water maze show?
- Test of spatial memory where the hippocampus important
- How long does it take for animal to reach platform?
- Once learnt where the platform is do a probe test: take out the platform, expect to search in training quadrant (where platform used to be)
- As increase does of drug (antagonist of NMDA receptor given in the training period) the animals search pretty much equally in all quadrants suggesting because they couldn’t carry out LTP memories for the task were not formed.
How can we show that reversal of LTP leads to forgetting?
- LTP maintenance depends on protein Kinase M delta therefore if this substance is blocked LTP cannot be maintained/ is reversed
- ZIP is a substance that can block protein Kinase M delta and we see that as it is introduced LTP levels drop drastically.
- In an experiment there is a circle with a quadrant where an animal will receive an electric shock after training animals have good retention at 24hr not going in the area where they will receive punishment (while machine is turned off- not getting continued stimulation/ cues). After ZIP is taken however, LTP is no longer maintained and they go back to rooming all over the wheel (they no longer have memory of where the danger area is).
- Therefore, it can be said that ZIP abolishes long term retention of spatial info
