HBY 554: 2/27: Synaptic Plasticity
Hebbs postulate
-where the term synaptic plasticity comes from -when cells are active, they end up becoming more active in the future (use it or lose it) -set themselves up to be more efficient to be better performers
sensitization of the sensorimotor neuron modulation lasts approx. how long? (similar to short term gill withdrawal produced by single shock to tail)
1 hour
In what 2 ways does CREB work?
1. Transcription factor/changing the activity of actual DNA (change through PKA activity being more persistent; receptor/channel changes) 2. sprouting new dendrites (structures/morphological changes)
steps in facilatory interneuron/sensory/motor neuron
1. tail is shocked and serotonin is released from the facilatory interneuron end to the pre-synaptic terminal of the sensory neurons 2. Serotonin binds to the serotonin g-protein receptors on the membrane 3. This activates the g-protein and causes it to disassociate from receptor and bind to other signaling molecules like adenyl cyclase 4. adenyl cyclase produce cAMP from ATP 5. cAMP binds to regulatory subunits of pKA, liberation catalytic subunits of PKA 6. These catalytic phosphorylate channels (like K+ channels, opening fewer) and allows for a greater influx of Ca2+ into the presynaptic terminal via their channels (due to phosphorylation). 7. This increase of Ca2+ causes more NTs to be released.
explain 2 examples of habituation with clothes and DLAR smell
1. when you first put clothes on, you can feel the cloth on your skin but throughout day, it mutes out 2. When you first go to DLAR, it smells but by the end of the week your nose pathways have been stimulated enough that you don't need to carry this message on forever.
2 post-synaptic cell receptors involved in LTP
AMPA and NMDA receptors
which post synaptic receptor has a more dominant current flow and of which ion?
AMPA/Na+
PKA activation of ___ produces long-lasting changes in synapse structure
CREB
whats stimulates increased degradation of PKA regulatory suits, allows pKA to be persisistently active
CREB
Ins synaptic facilitation, cells have identical strength but because of the ___, it's able to increase the strength in the second ap
Frequency
Eric Kandel used mollusks Aplysia to study what?
Long-term synaptic plasticity that underlie simple forms of learning
silent synapses only have what receptor?
NMDA receptors
Hebb's postulate in terms of LTP
Only strengthening the synapses that are stimulated
extensions of the CA3 pyramidal cell body is called ___ ___
Schaffer collaterals
what happens to AMPA receptors as a results of low calcium concentration in the postsynaptic cell? What happens to glutamate sensitivity?
They can becomes internalized and the glutamate sensitivity decreases
T/F: Maintenance of LTP occurs due to changes of gene expression and protein synthesis
True
what is a functional synapse?
a synapse that has both AMPA and NMDA receptors
in LTP, degrading the PKAs regulatory subunits allows it to be more ___
active
What kind of muscles can have facilitation and then depression?
anaerobic because it needs such exaggerate stimulation
What is the molecular mechanisms for why NMDA receptors by themselves won't work for synaptic transmission?
b/c NMDA receptors by themselves won't be able to bring any of the Na+ or Ca+ due to the mg2+ block which can only be unblocked by the depolarization of the membrane, which can only occur with AMPA receptors, known for being permeable to Na+
augmentation
bringing something back/recovery
increase in NT level= increase that synapse will experience ___
depression
in LTD, why/how do post-synaptic phosphates get activated?
due to low frequency stimulation which leads to low amplitude rise in calcium concentration
synaptic facilitation results from prolonged ___ of Ca2+ levels in the pre-synaptic terminal
elevation; doesn't get to recover so NT builds further
Drugs that block protein synthesis prevent LTP, but not the maintenance of it.
false, it prevents the maintenance of LTP, but not LTP itself
T/F: Schaefer collaterals have to be stimulated together
false, they can be stimulated separately
T/F: LTD and LTP have the same intracellular pathways, and if false, why?
false, they use different kinases to engage their respective responses in the post synaptic cell
LTP response is strongly correlated to the ___ of ___ ___
formation of new synapses
what NTs do sensory neurons release onto motor neurons
glutamate
What 2 types of cell are there in the hippocampal circuitry?
granule and pyramidal cells
repeated siphon stimulation causes the withdrawal reflex to weaken over time, also known as ___
habituation
Molecular mechanism for LTP
has both NMDA and AMPA receptors, Na+ flows into NMDA receptor. Increased amount of Na+ causes a depolarization of the membrane, which allows for the Mg2+ in the NMDA receptor to unplug and allows for the flow of Ca2+ and Na+. This increased influx of Ca2+ allows for the initiation of LTP to occur.
LTP associativity
if one pathway has a strong pathway and pathway puts a tiny amount of effort at the same time, they both can get strengthened.
in LTP, what can CREB do in terms of the amount of protein structures
increase the amount of protein structures, which can increase the sensitivity of the synapse
sensitization modifies the circuit habituated circuit as a shock will do what?
it will pair the aversive and non-aversive pathway and cause the facilatory neuron to release serotonin onto the presynaptic terminal of the sensory neuron
Habituation
less responsive to repeated occurrence of a stimulus
LTP: State dependency
need the pairing of the pre and post synapse to increase EPSPs
Short-term plasticity: Synaptic depression is related to the amount of ___ released and too much could cause ___
neurotransmitters, depression
short term synaptic plasticity is cells receiving a different quantity of ___
neurotransmitters; abundance or depletion of ligands
in habituation, over time from the siphon being touched, the sensory and motor neuron get depressed and their is decreased response due to a reduction in what?
number of synaptic vesicles available for release in axon terminals
LTP: Specificity
only the pathway that is active/action potential occurrence will cause the synapse to be strengthened
Sensitivation
pairing an aversive and non-aversive pathway to help make re-engage the non-aversive pathway to be more responsive to stimulus
Short term plasticity: synaptic facilitation is a ___-___ event where something gets helped along/moved along
pre-synaptic
the modulatory/facilitatory interferon actually connects to the ___-___ side of a mechanism
pre-synaptic
CREB is a transcription factor, which means
proteins involved in the process of converting, or transcribing, DNA into RNA.
Synaptic faction happens at what speed and is it reversible?
quickly and yes for the most part
In Synaptic depression, post-synaptic cells lose the amplitude of their ___
response
Short term plasticity: Post tetanic potentiation
response happens after stimulation has been removed so it takes longer to initiate the change also longer In response (delay onset)
in between which 2 neurons can their be habituation
sensory and motor (glutamate synapse)
the interneuron to sensory neuron is what kind of NT synapse?
serotoninergic
what is the mechanism behind how long-term synapticity works?
stimulation creates changes to how it'll behave in the future; change receptor expression and kinase expression
vesicle depletion hypothesis
there can be so much release of NT, that vesicles can actually be depleted of NT over time and won't be replenished until the mobilization of vesicles from a reserve pool
The ability of the synapse is...
to change in response to stimulus
Short term plasticity: synaptic facilitation is a ___ increase in synaptic strength that occurs when 2 or more action potentials invade the ___-___ terminal is close succession
transient, pre-synaptic
T/F: All neurons have to have facilitation before depression
true
T/F: When you change receptors due to long term plasticity on membrane, you change how the cell behaves to a fixed amount of neurotransmitters
true