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31 Cards in this Set
- Front
- Back
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6 biochemical mechanisms (used for memories) that can be graded by their volatility (the ability to change); high to low
depending on change, you can predict? high volatility= |
HIGH 1. changes in phosphorylation state (can easily be reversed by phosphatases) 2. insertion and removal of membrane proteins (reversible but requires energy) 3. persistent activation of protein kinase (used a lot for generating memory; reversibility depends on mechanisms for persistence ) 4. production of new proteins (requires constant energy, persists based on half life of protein/mRNA) 5. morphological changes at pre-existing synapses (making synapses bigger to transmit info better) 6. new synapses LOW
you can predict how long the memory will last
high volatility= the memory is easily changeable/removable through the mechanism
how long the memory will last |
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what are non-associative memories?
habituation for non-associative memories involves..... what about sensitization? |
it means there is no specific association between a conditioned and uncondioned stimulus (the stimulus alone is strong enough to trigger a memory )
habituation = the decrease in a defensive reflex due to repetitive non-noxious stimulation (CS alone)
sensitization= the increase in a defensive reflex due to a noxious stimulus (US alone; requires a noxious, you're not associating it with anything it just leads you to your knowledge where you're in a situation to which you have to be defensive ex scary movie) |
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why do we use the aplysia system in looking at the nervous system? (3) |
1. they have simple behaviours and simple neuronal circuits 2. neurons are large and identifiable bw preparations (can trace the ciruict underlying behaviour easily) 3. primary cultures of neurones can recapitulate the changes observed during behaviour (can analysis ) |
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how do we test sensitization and habituation of a memory in aplysia? |
for sensitization, a noxious stimulus to the head or tail will cause an increase in the time and extent of gill withdrawal to a touch to the siphon
for habituation, repetitive touches to the siphon causes a decrease in gill withdrawal; animals that live in tide pools who are always buffeted learn to ignore the stimulus |
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how can you measure synaptic strength (use EPSP and IPSP) |
action potentials cause the presynaptic cell to release neurotrans that acts as a ligand to open channels in the postysnaptic
you can measure Na+ for EPSPs and Cl- for IPSPs which are ions that flow into the postysnaptic cell (after depolarization) ; the PSPs are measured as a change in voltage in the postsynaptic cell
if you place an electrode in the posynaptic cell, fire an action potential in the pre synaptic cell, you can measure the strength of the synapse by measuring how much the voltage changes
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2 ways of semi-intact preparations to test that cellular mechanisms that mediate habituation of a gill and siphon withdrawal reflex :
habituation and sensitization changed the synaptic strength bw _____ and _________ |
1. headless- all nervous system except the abdominal ganglion is removed 2. immobilized preparation in which the nervous system is intact but the abdominal ganglion is exposed
sensory and motor neurons |
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in stimulating the sensory neuron and looking at the EPSP in the motor neuron and you continue to fire the sensory what happens?
what kind of stimulation do you have to do to get sensitization ? |
the synapse depresses rapidly= cellular depression underlies behavioural habituation
you have to shock the neuron --> large increase in the synaptic strength which means the same firing of the sensory neuron causes a bigger response in the motor |
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applying of 5-HT mimics ______ and causes ______
removing 5-HT containing neurones with a toxin ______ sensitization
5-HT containing neurons fire during _____
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mimics in the synaptic strength bw sensory and motor neuron
reduced (aka no longer sensitize if you remove serotonin)
serotonin neurons are fired during sensitization training and thus released during sensitization |
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behaviour habituation involves ______= cellular ________
behavioural sensitization involves ______ = cellular ________ |
repeated touches leads to decrease of withdrawal; depression which is repeated firing of sensory neuron that leads to less release and decrease of EPSP to a motor neuron vs involves shocking a tail or head leading to increase of withdrawal ; facilitation which involves shocking the nerve or adding serotonin leading to more release and increase of EPSP to motor neuron
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3 ways to increase synaptic strength
M= NPQ --> what the f does this mean |
1. releasing more transmitter/action potential
2. increasing the effect of releasing the same amount of transmitter by having a bigger post-synaptic response
3. having more synapses
M (strength of synaptic connection) = N(number of synapses) x P (probability of release of a synaptic vesicle after an action potential) x Q (amplitude of the EPSP resulting from the release of one vesicle) |
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how can we control the probability of release of synaptic vesicles after an action potential (controlling P)? (3) |
1. modulate the Ca+ channels to change the amount of Ca entering with an action potential (Ca+ comes in when vesicles are ready, changing the coupling can change sh**)
2. the number of vesicles that are ready to release (if no vesicle is ready they dont release any obvi, need a combo of vesicles at the active zone)
3. coupling of Ca+ entry to fusion of the vesicle |
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how do miniature EPSPs 'probe' for changes in P and Q (the probability of release of vesicle and the amplitude of EPSP)
changes in the amplitude of miniature EPSP indicates a change in _____ |
miniature EPSPs is the release of a single vesicle (in an absence of an AP the vesicles fuse at a spontaneous rate) - the more frequent these minis occur, the more readily releasable vesicles there are (vesicles more ready)
Q |
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habituation = ______ in P
why is there no change in the mini amplitude during habituation?
behavioural habituation = depression= ______ |
a DECREASE in the probability of release of a synaptic vesicle after an action potential
this means that there is no post-synaptic change; mostly due to calcium-secretion coupling aka less Ca+ is coming in during the AP ORRR the Ca+ dosnt cause release of synaptic vesicles
loss of calcium secretion coupling |
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how does short term facilitation depend on PKA? ( for presynaptic) (3) |
1. 5-HT acts through a G-protein-linked receptor to increase the levels of cyclic AMP (cAMP a 2nd messenger)
2. cAMP activates the cAMP-dependent protein kinase (PKA; a protein that acts by modifying other molecules through adding a phosphate group)
3. PKA phosphorylates a K+ channel and inactivates the channel (usually the channel stops the actions of Na+ and Ca+ channels so inactivating it makes the cell DEPOLARIZE)
** AP broadening = more Ca+ coming in = activated by depolarization = more flows in = more neurotrans = more the post synaptic depolarizes = bigger response of muscle |
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how does short term facilitation depend on PKA contd ? (post synaptic) (4) |
4. inactivating K+ channel= depolarization of the AP (the depolarization lasts longer)
5. broadened action potential= INCREASED Ca+ influx
6. leads to more transmitter release/ AP (which is sensitize to the 5th power of Ca+ concentration)
7. more transmitter release = increased EPSP bw sensory and motor neuron (more withdrawal of gill and siphon, more AP of the motor neuron) |
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what is a memory trace?
the memory lasts as long as the site remains ________
short term sensitization/factilitation lasts about : |
the PKA phosphorylation of the K+ channel is the trace
remains phosphorylated
20-30 mins |
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what happens if you preent the action potential from broadening by voltage-clamping the neuron?
how can 5-HT increase vesicle release? |
it reduces BUT DOES NOT REMOVE the increase in EPSP after adding serotonin
by modifying priming or docking or coupling to calcium as well as action potential broadening |
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how does an increase in priming cause facilitation? ; what are the 2 different kinases that mediate this?
PKC is important for ____ and _______. |
an increase in the priming of vesicles causes an increase in the frequency of minis during facilitation (no effect on amplitude)
this is mediated by protein kinase C (PKC) and protein kinase A
important for the reversal of depression and increasing calcium-secretion coupling |
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explain the relationship bw increased behaviour,increased excitability and K+ channels |
increased behaviour is due to increased excitability - inhibiting K+ channels depolarizes the sensory neuron so it requires less stimulation to fire and it also leads to less resistance to firing repeated action potentials (same stimulus leads to more APs)
this demonstrates that its not just synaptic, when more sensory neurons fire there are large EPSPS in the motor neurons which leads to more withdrawal |
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cellular consolidation vs systems consolidation in the memory field |
cellular= how changes at the cellular level last for a long time vs how memories can move from one system to another (moving temporary store in the hippocampus to permanent store in the cortex) |
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what are some advantages of the Aplysia system in looking at long term memory formation (2) |
1. it can identify specific synapses that change during behavioural memory 2. you can reconstruct the synaptic modifications in cell culture which allows you to have a powerful experimental model for cellular memory |
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differentiate between the different memory phases in sensory-motor neuron plasticity:
Short term facilitation (STF) intermediate facilitation (ITF) long term facilitation (LTF) late long term facilitation (L-LTF) |
STF= 0-30min; is due to activation of protein kinases by 2nd messengers (cAMP) that lead to INCREASE in transmitter release ITF= 30min-3 hrs; its independent of gene expression and depends on persistent kinase activity and translation of pre-existing mRNAs into proteins LTF= 3 h- 1 day; is blocked by inhibitors of RNA transcription (gene expression) and occurs during induction but not the expression of long term facilitation L-LTF= more than 1 day, may require the formation and stabilization of new synapses
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what morphological changes with long term sensitization correlates with increased number of synapses ? (3)
however, as memory persists only _______ persists |
changes such as: 1. increased size of active zone, 2. increased docked vesicles 3. increased number of synapses
the increased number of synapses persists, memory is encoded and increased in the NUMBER OF CONNECTIONS |
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serial va parallel memory formation with the analogy of LTM as a brick house |
serial= one memory makes the frame of the house (short term), puts in the plaster and walls (intermediate) then lay the bricks (LTM); it fits with the term consolidate (becoming stronger and more stable) - the LTM depends on the STM
parallel= 3 little pigs, one starts building a straw house (STM), a stick house (intermediate) and a brick (LTM) all at the same time; the brick house takes a long time so one needs he other houses so there is somewhere to live in between (memory is continuous)
BOTH OF THESE ARE TRUE |
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what is a major feature bw memoirs that only last a short time vs memories that persist
why might gene expression (protein synthesis) may actually not be necessary for LTM? (2)
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the requirement of gene expression!! ; this is now used to mark neurons that participate in long lasting memory
1. gene expression only occurs in the nucleus and memory is stored at synapses 2. gene expression isn't instructive (how does gene expression know which synapses to change)
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what are transcription factors? 2 ways they regulate gene expression |
they are genes transcribed into RNA only at appropriate time and that bind to transcription factors - they seek codes that are in the DNA which tells the factors to bind to the DNA and recruit the machinery to make mRNA
1. they recruit the enzymes that make RNA from DNA (RNA polymerase) 2. they alter the structure of the DNA to open it up by modifying histone (activators acetylate histones and repressors de-acetylate histones) |
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what transcription factor is required for long term facilitation? how was this discovered
CREB only binds when |
CREB (cAMP Response Element Binding Protein) ---> it was found that when cAMP is rewired to make LTM, cAMP can activate transcription through CREB
when learning happened (it got activated by learning) |
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CREB activity is regulated by 2 factors:
2 things required for transcription: |
1. CREB will only recruit RNA polymrase when its phosphorylated
2. CREB acts as a dimer (a molecule complex that has 2 identical molecules linked together); it can dimerize with an inhibitory protein called a CREB repressor _________________________________________ 1. activation of CREB kinases 2. removal of CREB repressor |
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explain the relationship bw the CREB repressor and the CREB activator
reducing CREB repressor results in? |
CREB activation is regulated by tho ratio - reducing CREB repressor shifts the balance to easier activation of CREB but still needing stimulation
= long term facilitation from a stimulus that normally only led to short term facilitation |
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evidence that CREB is important for long term memoirs (5) |
1. over expression of a CREB inhibitor blocks long term door avoidance memory 2. removal of CREB repressor in vertebrates allows LTM to be formed easier 3. CREB knockouts have impaired LTM for fear avoidance, water maze and social recognition 4. removing CREB acutely blocks LT taste aversion and water maze consolidation 5. overexpession of CREB converts a stimulus that doesnt usually lead to LTM of fear avoidance to one that does |
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what happens if CREB is overexressed in a subset of lateral amygdala neurons using a virus that transduces 20% of LA neurons?
what happens if you kill these neurons as well as CREB? ^^ |
the CREB expressing neurons are more likely to turn of IEG (Arc) after behaviour than non-expressing neurons
the memory is erased, which suggests that the memory is encoded in the same neurones that gene expression was activated in!!! ** memories made before the expression of CREB remains intact |
