learning and memory (anton) Flashcards
(41 cards)
define
1. learning
2. memory
3. recall
4.the engram
Learning = acquisition of information
Memory = storage of learned information
Recall = reacquisition of stored information
The engram = physical embodiment of a memory
what is procedural memory?
Skills and associations we do unconsciously - like riding a bike, playing an instrument i.e. you don’t have to think about it
what is declarative memory?
Can be encoded in symbols and language - available to conscious mind
what is explicit memory?
memory that can be consciously recalled (e.g. recalling riding a shiny new bike on the Christmas day when you were 5)
what is implicit memory?
Implicit memory
Memory that cannot consciously recalled (e.g. learning to ride a bike)
Can be different types:
Includes procedural memory
Classical conditioning (associating a stimulus with a behaviour)
Priming (when one stimulus influences the response to subsequent stimuli)
what animal is used to show habituation and sensitisation?
the aplysia snail
has a siphon (tail? idk)
and delicate gills it hides if hurt/sensing danger etc…
what neurons are involved in the gill withdrawal reflex and how is habituation shown?
Sensory neuron (presynaptic) of the syphon skin synapses with a motor neuron (L7) resulting in gill withdrawal
researchers poke the syphon, and eventually the aplysia stops withdrawing its gills when it realises the pokes aren’t harmful
what did recordings from the presynaptic sensory neuron and the L7 motor neuron show?
what can this be concluded about where the memory is learnt/stored?
Response at the postsynaptic neuron is reduced as number of pokes (stimuli) increases (while the presynaptic neuron maintains a steady response)
This means the ‘memory’ is learnt somewhere after the body of the presynaptic and before/at the body of the postsynaptic
in habituation, we know that the memory (of ‘no harm’ in this example) is learnt after the presynaptic neuron.
so what is the mechanism of habituation?
when looking at vesicles of NT released at a synapse, you have three populations:
- Readily releasable pool (attached to active zone)
- Proximal pool (very close but not yet docked)
- Reserve/resting pool (a bit further away, takes longer - mins - to be released)
The proximal pool takes some time to dock (reserve pool even longer), so…
Increasing repeated stimulation will result in reduced response as the readily releasable pool has been depleted and the reserves need a little bit more time
what is the procedure to investigate sensitisation (in aplysia)?
Application of a painful/noxious stimulus alone (e.g. shock to the tail) then results in a benign stimulus (e.g. poke of the syphon) eliciting a stronger response (faster/longer withdrawal of the gills) when this benign stimulus would have previously caused habituation
what neurons are involved in sensitisation in aplysia?
got the sensory neuron at the syphon synapsing with the motor neuron L7 of the gills, but the sensory neuron ISN’T being activated (at first)
Additional ‘interneuron’ involved, activated by the painful stimulus being applied - the L29 neuron
what are the mechanisms occurring in sensitisation?
the painful stimulus activates the L29 interneuron
Its presynaptic terminal releases serotonin to act on the sensory neuron just before said sensory neuron synapses with the motor neuron L7
Activation of receptor on sensory neuron causes it to produce adenylate cyclase → cAMP → PKA
More PKA in the presynaptic sensory neuron causes phosphorylation and therefore inactivation of K+ channels, slightly depolarising the membrane…
When a gentle poke is then applied to the syphon, more NT vesicles are released from sensory neuron at the same time because of the slower repolarisation, so there is more activation of motor neuron = larger withdrawal of the gill muscle (protecting it’s sensitive parts)
what is the mechanism/s occurring during this process of associative learning?
You’ve got the ^^sensitisation mechanism occurring due to the pain (US): L29 releasing serotonin causing adenylate cyclase activation → more cAMP → PKA phosphorylating and inactivating some K+ channels etc…
AT THE SAME TIME - sensory neuron is being activated
Increases intracellular Ca2+ in the sensory neuron terminal, the Ca2+ provides +ve feedback to adenylate cyclase that’s being activated due to L29 neuron, produces even more cAMP, causing a larger response
is it that simple (sensitisation and associative learning mechanisms)?
There are more things going on -
Complex models of sensitization and learning:
Multiple intracellular signalling pathways are needed, pre and postsynaptic
Long term phase involves the nucleus and altered gene expression, uses proteins like MAPK. early phase uses other pathways like PKC, and AMPA and NMDA receptors etc…
Hebbian synapse?
Coordinated activity of a presynaptic terminal and a postsynaptic neuron strengthen the synaptic connections between them
suggesting that when two neurons are repeatedly and persistently activated together, the strength of the synaptic connection between them increases. Summarised as “cells that fire together wire together,” basis of associative learning and memory
hippocampus and memory?
Involved in memory
First realised due to it being affected in Alzheimer’s
Taxi drivers have a larger hippocampus - spatial memory
what simplified circuit was investigated in the hippocampus?
Entorhinal cortex → dentate gyrus = perforant path synapses
Dentate gyrus → CA3 = mossy fibre synapses
CA3 → CA1 = Schaffer collateral synapses
investigating LTP -
which neurons were looked at, what was done to them and what was observed?
Stimulate enough presynaptic mossy fibres (CA3), measure effect on postsynaptic CA1 neuron (so we are looking at Schaffer collateral synapses)
A high frequency presynaptic stimulus produces long lasting-potentiation -
- Stimulus causes an EPSP
- A continuous high frequency stimulation (100 stimuli/sec) resulted in larger amplitude EPSPs being produced. I.e. the HFS (high frequency stimulation) has caused a modification of the stimulated synapses so that they are more effective
This effect can remain for days, weeks, or even years (tho ‘years’ is hard to prove)
when looking at LTP what is meant by input specificity?
what does this suggest about where the LTP mechanisms occur?
Input specificity - e.g. if a neuron had two different inputs. You only stimulate one of them with high frequency
Only stimulation of this input showed increased amplitude EPSPs
Stimulation of the other input that wasn’t ‘trained’ did not show any difference in EPSP
Suggests the mechanisms involved don’t happen at level of CA1 (post) cell body, but most likely at synapse
high frequency stimulation results in LTP when…?
High frequency stimulation results in LTP when it causes temporal summation of the EPSPs
what is meant by cooperativity?
this demonstrates LTP can occur by ways other than temporal summation as seen with HFS)
Cooperativity = Two pathways converging on the same target can both be strengthened if they fire together (basis for associative learning)
Don’t need high frequency stimulation to cause LTP necessarily. If multiple synapses are active at the same time, they cause spatial summation of EPSPs, and EPSP amplitude was also seen to increase when the pre and postsynaptic neurons were stimulated at the same time
what are the three kinds of glutamate receptors, including what they do?
AMPAR = slightly selective for Na+ ion channel, opens and depolarises neuron when Glu binds
NDMAR = Glu binds, ion channel selective for Ca2+ - doesn’t necessary depolarise the cell a lot, but causes downstream effects
there is a Mg2+ block, where despite Glu being bound, it prevents channel opening (it is removed by depolarisation)
mGluR = activated - G protein signalling cascade (not relevant here)
CA3 - CA1 neurons -
what do we see in LTP (on a molecular level) and what is needed for this change to happen?
In LTP we see an inc. in number of AMPA receptors at postsynaptic membrane
To get this effect at the postsynaptic membrane…
Presynaptic needs to depolarise in order to release glutamate
Postsynaptic also needs to be depolarised at the same time, in order to remove the magnesium block on NMDA receptors
Opening of NMDARs = Ca2+ in, downstream effects causing increased gene expression of AMPARs
