Lecture 21- Molecular mechanisms of memory Flashcards
Where is the hippocampus?
-primitive part of cerebral cortex located medially in temporal lobe
When is the hippocampus active?
during consolidation phase of explicit memory
What does the failure of consolidation result in?
-no formation of long term memory -appears in alzheimer’s
What happens when the hippocampus is damaged?
- prevents formation of new long term explicit memories but does not disturb already formed memories -Does not prevent formation of implicit memories (but can’t remember how you formed them)
What role does hippocampus play in explicit memory?
-central to explicit memory= cannot form it without it -the transmission from working memory to explicit long term memory -becomes active again during the consolidation process (when you’re asleep) -part of tuning of memories, need to be able to weight the balance of memories, what happened today, yesterday etc.
What does it mean that memory is associative?
-have a memory but also lot of facts surrounding it, = pulling one element then brings things associated with it.
What is a characteristic of explicit memory?
-it is associative -related information is recalled together
What happens when you’re recalling a memory?
-Recall of stored memory of an event activates parts of cortex activated when the event was sensed – The event is partially relived
What is the role of the neocortex in memory?
-storage
What happens during long term memory formation?
-During long term memory formation (takes days) continual interaction between neocortex and hippocampus -after a while you don’t need the hippocampus to recall the memory,
How is memory stored?
-as strength of connections between neurons in a network
Is memory dependent on individual neurons?
-Individual neurons can participate in several memories -Distributed, rather than depending on single neurons -Usually located close to the region that responds to a specific modality
What is sparse coding?
-one neuron per memory not true, more neurons involved in one memory, can multiply the numbers of memories you can have
What is the structure of memory?
-this is not only for neurons -collection of neuron-like interconnected elements -when give a stimulus then all will be activated (the ones that are sensitive to it) -interactions between the neurons get stronger and stronger -consequence is when stop the training stimulus= but not they are strongly interconnected and activating one will activate the others -partial activation gives the complete original stimulus =associative memory -memory is a natural consequences of having neurons taht can change the connections between them in response to repeated stimuli
What is long term potentiation? (Hebbian modification)
Long term activity dependent plasticity that satisfies the criterion that synapses strengthen when pre- and post-synaptic neurons are active at the same time -Long term potentiation (LTP) -one neuron active at the same time as postsynaptic nerons= that strengthens the connection LTP -with repetition becomes a memory trace
What is long term depression?
-(LTP) is another form of Hebbian modification -where presynaptic and postsynaptic neuron are not active at the same time= then less connection! LTD
What is neuronal scaling?
LTP= even though synapse gets stringer, adjustment (neuornal homeostasis) to frequencies, so when the connection stronger the firing stronger but not that much neuronal scaling= brings the synapses to appropriate level, so the connection not too strong
What does this picture show?
-LTP -frequency is the test -tetanus= high frequency stimulation is applied to the axon 1, the size of the output is increased after this -the effect lasts for up to a month =if put the same input to input 2 then not increased -the neuron remembers that only input 1 was stimulated
What does this picture show?
-LTD -give stimulus that is not strong enough to activate the neuron -then the response gets smaller, this effect lasts long = LTD -remembers that this input is ineffective -the other set of inputs doesn’t get activated -associated already
What is the postsynaptic mechanism for LTP?
1.-glutamate excited AMPA receptors (Na+ going in) 2.-the depolarisation unblocks NMDA receptors 3.-Ca2+ going in through the NMDA 4.-Ca2+ activates dependent kinases 5.-the kinases phosphorylate AMPA receptors or cause insertion of AMPA receptors into the terminal membrane -thus the cell is more easily excited by glutamate now -more activation -happens on the postsynaptic terminal on synaptic spines
What happens to CaMKII when Ca2+ influx?
1.-normally the hinge like subunit of CaMKII is off 2. the hinge opens upon binding of Ca2+- bound calmodulin, freeing the catalytic region to add phosphate groups to other proteins 3.large elevation of Ca2+ can cause phosphorylation of one subunit by another (autophosphprylation) which enables the catalytic region to stay on permanently
