consolation and synaptic plasticity - week 2 Flashcards
timescales of memory
memories can persist for different lengths of time depending on underlying mechanism
memories can be localised to specific areas of the brain, take time to stabalise and are likely to be supported by synaptic plasticity
- pavlovian fear memories in the amygdala
memories can be supported by decreases in synaptic strength
- motor memories in the cerebellum
visual memory
can be separated into 3 stages
iconic
short term memory
long term memory
iconic memory
less than 1 second
likely to result from brief after images in the sensory neurons of the retinal surface in the eye
demonstrated with the sperling array
short term memory
retention of information over a period minutes to hours
poorly defined concept
generally thought that the biological mechanisms of s-t memory commonly include sustained neural activity
- persistent neural activity can sustain STM
in monkeys
- electrophysical recordings showed that the activity of neurons in the visual association inferior temporal cortex which were sensitive to a particular complex visual stimulus actually outlasted the presentation of the stimulus
long term memory
can last up to a lifetime (24 hrs)
depends on specific areas within the temporal lobe
fear conditioning
type of pavlovian conditioning
includes the formation of an association between a previously meaning stimulus and an aversive outcome
subsequent exposure to the now fear-conditioned stimulus results in fearful behaviour
fear conditioning - what is the main brain area implicated
amygdala
encoding long lasting memories
persistant neural activity sustains STM eventually this dissipates yet the memory remains intact for much longer
notion that STM is stabilised into a LTM may be inaccurate
- certain studies show that is STM is impaired LTM still forms
- so perhaps the mechanisms of LTM are triggered directly by the learning event in parallel with sustained neural activity
what distinguishes LTM and STM
differing dependence upon the synthesis of new proteins
mechanism for memory consolidation
what shows synthesis of protiens is needed for memory consolidation
anisomycin - prevents protein synthesis
can be infused directly into brain of rats at levels that almost completely prevent the synthesis of any new protiens for several hours
intra-amygdala infusion of anisomycin before or soon after pavlovian conditioning selectively disrupts LTM while leaving STM intact as shown in fear conditioning
also increased gene expression triggered by learning
- reasonable to suggest that specific protiens encoded by their up regulated genes might be required for consolidation
mechanism for memory consolidation
what protein
the activity - related cytoskeletal - associated protein (Arc) is simply up regulated in the amygdala following pavlovian fear conditioning
when synthesis of arc is selectively inhibited in the amygdala, the consolidation of the fear memory impaired
mechanism for memory consolidation
mechanism that translates behaviourally induced electrical signals in brain into gene expression
one of the direct regulators of arc expression is the ERK/MAPK signalling pathway
mechanism for memory consolidation
ERK/MAPK signalling pathway
this pathway consists of a series of kinases
these are protein enzymes that function to phosphorylate other protiens
this causes their enzymatic function to be activated
leading to the activation of further downstream mechanisms in the pathway
the same study that the upregulation of arc following fear conditioning also showed that this upregulation was dependent upon ERK/MAPK signalling
- as expected the inhibition of ERK/MAPK signalling also impairs the consolidation of fear memories in the amygdala
mechanism for memory consolidation
NMDA receptor
glutamatergic receptor
upstream of ERK/MAPK pathway the primary cell surface receptor involved in learning in the NMDA receptor
heavily implicated in learning with links to ERK/MAPK pathway
mechanism for memory consolidation
NMDA receptor - evidence
direct infusion of NMDA receptor antagonism AP-5 into the amygdala blocks the acquisition of fear conditioning
blocks LTM
also impairs STM
- suggest NMDA receptor is critically involved in memory acquisition
- divergences downstream mediating STM and LTM