Neural mechanisms of pavlovian conditioning

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chloride ions have what charge?
negative charge
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sodium ions have what charge?
positive charge
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predominance of charge inside cell?
negative charged ions
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predominance of charge outside cell?
positive charged ions
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resting potential?
-70mv
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what is a synapse?
terminal button at the end of the cell
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what is the presynaptic membrane?
its on the neuron sending the message
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what is the postsynaptic membrane?
on the neuron receiving the info
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what is EPSP?
excitatory depolarisation of the postsynaptic membrane
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what is IPSP?
inhibitory hyper-polarisation of the postsynaptic membrane
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explain excitatory changes in potential.
sodium goes through the ion channel from outside into the cell, influx of pos charged sodium into the cell produces depolarisation
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explain inhibitory changes in potential.
ion channels allow potassium to flow out of the cell (negatively charged), so inside becomes more negative and hyperpolarises
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what is the role of calcium ions?
when they flow into the cells they don't change much of the potential - it acts to activate enzymes
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how did Lomo (1996) define LTP?
intense electrical stimulation of preforant path from entorihinal cx to dendrate gyrus
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how do you measure synaptic response over time?
before stimulation you have a short number of bursts (100hz pulses), with repeated firings, and then give a single burst and the response is x3 bigger - massive effect of depolarisation, lasts longer, over time magnitudes increases/long term increas
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what did Kelso, Ganong & brown (1986) do? (LTP)
depolarised CA1 neuron and stimulated different axons, strengthening synapses and depolarised - LTP requires simultaneous depolarisation of postsynaptic membrane & activation of synapse
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what does drug AP5 do?
blocks NMDA receptors, blocking influx of calcium ions into cell & blocks LTP - more AP5 less LTP
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what is NMDA?
specialised ionotropic glutamate receptor that controls calcium channel that is normally blocked by Mg2+ ions - it has ionotropic properties and is opened by glutamate
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what happens when there is an influx of Ca2+ into the cell?
if calcium flows into cell its important as a messenger to activate CAM-KII enzyme
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what happens if dont have type 2 calmodulin kinase? (-CaM-KII enzyme)
this enzyme mimics the effects of LTP so mice without it dont show LTP - inhibitors impair LTP in vitro
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what is NO synthase and where is it found?
enzyme that promotes production of NO - and drugs that block this prevent LTP - found in dentate gyrus, CA1, and CA3
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what happens to the synapse in LTP?
increase in number of receptors on postsynaptic membrane, so more receptors can open and increase of influx of ions into cell (excitatory)
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what happens when insert additional AMPA receptors into postsynaptic membrane? (Shi et al 1999)
control sodium channel - insert gene for AMPA receptors into rat hippocampal neurons - before LTP receptors are at base of dendritic spines and after move to synapses (this was blocked with AP5)
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what other changes were found when inserting AMPA receptors?
production of new synapses, change in size/shape of dendritic spine, and presynaptic changes (increase of glutamate released)
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what is long lasting LTP?
more than a few hours and requires protein synthesis
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what did Frey et al (1988) do? (long-lasting LTP)
blocked protein synthesis before, during or immediately after tetanic stimulation - LTP normal but disappeared after few hours - but when they blocked it 1 hour after stimulation the long lasting LTP was ok
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what is E-LTP?
early STM - produced by single high frequency train of stimulation (lasting less than 1 hour) - immediate changes caused by insertion of AMPA receptors
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what is L-LTP?
longer term memory - produced following consolidation & by multiple high frequency trains of stimulation (LTP2 lasts 1-3 hours/involves local protein synthesis) (LTP3 lasts more than 4 hours & PS)
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what is the tag hypothesis of L-LTP?
LTP is established at a particular synapse - chemical tags are produced and a message is sent to nucleus to produce proteins which are then captured by tags to trigger L-LTP
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what is reconsolidation?
presenting a CS activates the CS-US memory - reactivated memories need reconsolidating into LTM
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what did Nader (2000) find? (reconsolidation)
infusing anisomycin (protein synthesis inhibitor) into the amygdala that impairs fear conditioning
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what is long term depression? (LTD)
long term decrease in excitability of neuron to particular synaptic input, caused by stimulation of terminal button which pos synaptic membrane is hyper-polarised/sightly depolarised
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pulse trains with higher frequency than 10hz cause what?
LTP
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pulse trains with lower frequency than 10hz cause what?
LTD
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what does LTD involve?
decrease in number of NMPA receptors on postsynaptic membrane and involves NMDA receptors - its also a low frequency pulse that produces prolonged increase in CA2+
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what is the Hebb rule?
the cellular basis of learning involes strengthening of a synapse that is repeatedly active when the postsynaptic neuron fires - the strong connection between neuron that receives stimulation & activates the neuron responsibly is why we have CC
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example of strong synapse and weak synapse
strong: puff of air to eye that activates neuron in somatosensory neuron causing you to blink. weak: 1000-hz tone that activates neuron in auditory system
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what is associative LTP and how do we get it?
we have a weak and strong connection to the neuron - when these are stimulated simultaneously, we make the weak synapse stronger as it releases glutamate and opens NMDA receptor and results in entry of CA2+ into cell
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what happens when have stimulation of weak synapse?
before and after it is the same (no change)
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what happens when there is stimulation in the weak and strong synapses?
increase in both excitatory postsynaptic potentials (increase in depolarisation in both)
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what happens when stimulation of just the strong synapse?
dont get a change in the weak synapse but do in the strong synapse (excitatory increase)
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how do you get a conditioned emotional response?
a tone (CS) is received in auditory cortex and aversive pain stimulus detected in somatosensory cortex - this projects to amygdala and more specifically the LN - strengthening weak synapse and pairs CS and US
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evidence of LA involvement in CER?
increase in number of neurons in lateral nucleus of the amygdala in response to a tone - correlation between firing rate of LA neurons and magnitude of CER in rats - if infuse drug that blocks subunit of NMDA receptors (eg. AP5) rats didnt show CER
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how does fear conditioning affect AMPA receptors?
AMPA receptors are driven into dendritic spines of synapses between LA and auditory axons
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what do neuroanatomists study?
wiring diagrams of the brain to trace directions of info flow from prima sensory neurons to higher-order areas
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order flow on info involving hippocampus?
main input to hippocampus comes from entorhinal cortex which receives input from high order cortical regions relating to all sensory modalities - so it receives highly-processed input
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what are place cells important for?
spatial memory (like a map)
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explain the morris watermaze experiment
rat in box filled with opaque water - hidden platform that allows rat to escape - once learns location of platform it then swims straight to it - if divided into 4 quadrants control rats swam to right quadrant, lesioned rats swam in circles
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define the US, CS, and CR of the watermaze
US is escape, CS is place, CR is approach to place
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how did they measure fear conditioning?
training stage: rat placed in novel context/hears tone/receives shock. conext test: animal returns and test for freezing behaviour upon tone - hippocampal lesion they learned the tone not context (HC lesions impair context learning not discrete cues)
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what is autoshaping?
it is learning about discrete cues: CS+ is paired with food and the CS- isnt paired with food - with differences in spatial location
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what does evidence of autoshaping suggest?
good model to investigate pavolvian - HC lesioned animals better at this than sham - hippocampus involved in learning about complex stimuli but not necessary for appetitive/aversive US's
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how is the nucelus accumbens structured?
two parts: core and shell - connect to VP and MD thalamus which then connect to anterior cingulate cortex which connect back to core of nucleus accumbens
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what happens when NA core is lesioned?
animals dont learn to discriminate CS+ from CS-
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what happens when the NA shell is lesioned?
nothing - the shell has no role in pavlovian conditioning - just the core - so they have different functions
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what is the dorsal subiculum and is it involved in PC?
part of the outer structure of hippocampus - little difference between lesion and sham - so core doesnt use info from here
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what is the ventral subiculum and is it involved in PC?
part of outer structure of hippocampus and showed no effect
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what conclusions do we therefore make about subiculum?
it has no impact on autoshaping so there must be a different output structure of hippocampus involved
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what other structure may be involved in PC?
entorhinal cortex projections to the anterior cingulate cortex
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what is the amygdala?
heterogenous structure (basolateral and central nucleus) - heart of limbic system involved in fear conditioning
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what is the central nucleus of amygdala responsible for?
autoshaping
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what is basolateral nucelus necessary for?
nothing - in sham and lesioned animals found both learned to press lever but the animal arent encoding the identity of the CS (behave as stimulus-response animals)
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what is the anterior cingulate cortex?
part of limbic cortex - projections to ventral striatum, basolateral amygdala and central nucleus
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what is anterior cingulate cortex necessary for?
autoshaping and possibly inhibiting CS- responses - cant learn and withhold info that CS- involves no food so it could be used to inhibit these responses
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what happens when anterior cingulate cortex is lesioned?
produce impairment of autoshaping - in sham make sensible response for CS+ but lesioned cant discriminate CS+ from CS-
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what is required to do PC well?
be able to discriminate between CS+/- and if can withhold inappropriate responding, make appropriate responses and detect reward and update representations to change behaviour
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predominance of charge inside cell?

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resting potential?

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