memory Flashcards
the engram (slightly outdated)
physical embodiment of a memory
collection of all changes that happen that lead to memory of information
procedural memry
thinking about how you are doing something activates the prefrontal cortex which can inhibit the procedural process while doing it
working memory where?
prefrontal cortex
hippocampus
essential for converting short into long term
declarative
ancient greek for seahorse
amygdala
multple, processed sensor inputs (smell)
implicit/emotional/learnt fear
lesions in hippocampus
cause memory loss
structure of hippocampus
3 layered cortex
Inputs from entorhinal cortex and beyond
Outputs to many regions via fornix
invaginatin
different types of cells in each layer
reverberatign circuits
constant activity of sets of neurones (which can be triggered by other events)
the hebbian synapse concept (more recent)
activity modifiable,plastic synapse
change in the synapse between neurones (simultaneous firing (fire together , wire together)
faciliations
synapse becomes strogner
depression
synapse becomes weaker (not always bad- can lead to acquisition of memory,not always forgetting)
immeditate
depend on depletion vesicles in presynaptci cleft
if not enough of them- can lead to depression of synapse
facilitation/depression
short term - mins/horus
ca2+ avilablilty /vesicles depletion
long term facilitation/depression
sustained (days/weeks+)
long term potentiation in hippocampus
a long lasting strengthening of synapse between nerve cells
long lasting increase in the number of AMPa receptors in the postsynaptic membrane
CA1 neuron connected with CA3 with a synapse
tetanic LTP
high frequency stimulation 1000 hz
Amplitude of EPSP will increase
This change can last for years
Specific to the input ‘input specificity’
By this the post synaptic neuron can store more informatin
Doesn’t necessarily only happen in the brain
If simultaneous dopelarisation two neurones at same time either side of synpase – increase in amplutide of ESPS and long term potenialtion
paired LTP
conincident stimulus and depolarisation
associativity
pavlovs dogs
Aplysia Californica
gill withdrawal reflex
Gill withdrawal reflex – they don’t like the gill to be touched
But if touched It withdraws
But it’s not a static process it may change
Gill withdrawal refelx
shows habituation short term sensitisation long term sensitisation classical (pavilion) and operant (skinner) conditioning
habituations
if keep touching gill the animal overtime will stop withdrawing the gill because will release it’s not dangerous //stop responding
short term sensitisation
couple touching gill with mild electric shock
- habituation
Pair single tail pinch (aversive) with siphon touch
Re-establish siphon reflex
Short-term ~60min+
Gills
have big neurones and simple nervous systems
long term sensitisation
repeatint pairing of siphon touch and tail pinch
long term non habituating siphon/gill refelx
LTP, LTD and Aplysia
Require receptor activation (glutamate / serotonin)
Altered synaptic responsivity
Mediated by second messengers (Ca2+/cAMP)
Require protein phosphorylation changes in early stages
Require protein synthesis for late stages
Involve biochemical and structural pre and post-synaptic changes
how does LTP occur?
evidence suggests often a post synaptic event
most indicates a critical role for Ca2+
involves trafficking of AMPA receptors to the postsynaptic membrane
Ampa recepors on postsynaptic membrane translocate//increase and increaser responsivity – leading to long term potentiation
Kluver Bucy syndrome
amygdala lesions
the papez circuit
visual and tacile agnosia
hypoerorality
hypoer exploration
herphagia
hypoersexuality
to achieve long term potentiation
same amount of glutamate being released from the presynaptic neurone evoking a greater response at the post synpatic neutron
which is achieved by an increase in number of AMPA receptors present on the post synaptic membrane
this increases the likelihood that a glutamate ovule will interact with an AMPA receptor causing it to open and intimate an EPSP in the post sync membrane
