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61 Cards in this Set
- Front
- Back
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What is synaptic plasticity?
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Changes in strength of a synapse
due to depression or enhancement |
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Alterations in synaptic strenght due to molecular mechanisms is called:
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Synaptic plasticity
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Why is the history of a synaptic terminal so important
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Depending on when and how much it fired will determine if it fires stronger or not.
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Synaptic strength refers to the amount of change of post synaptic membrane potential made by a single presynaptic A.P. How is this related to ion conductance, and bang for your buck?
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The change of the postsynaptic membrane potential is the change in ion conductance, and bang for your buck refers to how much change per pre synaptic AP.
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What are two types of short term change ins synaptic strength
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Synaptic enhancement and synaptic depression
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How can you tell the difference between burst temporal summation, synaptic enhancement and synaptic depression,
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The burst is about the same size, enhancement is larger "facilitation" and the depression results in lower changes in synaptic strength.
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When an AP is enhanced or depressed for short term, the degree (or length) of that enhancement or depression is broken into 3 categories: WHAT R THEY?
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Facilitation less than a second
Augmentation several seconds potentiation: a few minutes |
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potentiation?
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several minutes of enhancement that outlasts the initial train of A.P
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augmentation:
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the time span in which an enhancement or depression outlasts the initial train of AP during short term synaptic enhancement/depression
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How is Facilitation augmentation and potentiation triggered?
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By the buildup of Ca+2
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For short term synaptic enhancement there may be residual Ca+2 that allows for "facilitation, augmentation, and potentiation Why is this able to happen? Why does this Ca+2 become important?
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it takes a while for the pres-synaptic terminals to restore Ca+2 levels.
Ca+2 trigger release of NT synaptic vessicles, and Protein kinase to increase the pool of releasable vessicles. |
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What are the 3 possible mechanisms for short term synaptic depression?
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Vesicle depletion
Ca+2 accumulation Feedback mechanisms |
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How does vesicle depletion result in short term synaptic depression?
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If a presyaptic cells recent history had released NT vescicles then there will be fewer vescicles available during AP to be released since they were already released before
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How does feedback mechanisms result in short term synaptic depression?
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if cannabanoid of the postsynaptic cell releases a retrograde signal to the G-Coupled protein receptors of the presynaptic terminal. This in turn inhibits the NT releasal. Also auto receptors that pick up feedback from the excessive NT release (are also g-coupled protein receptors) can inhibit NT releasal. They do so by opening K+ channels and that cause hyperpolarization.
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Associative vs non associative learning
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The short term changes (depression/enhancement) are non associative learning: They are time dependent and activity dependent changes due to single stimulus:
Associative learning is more frequent which involves paring two or more events that occur at the same time. |
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Two types of associative learning that was discussed in class:
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Pavlovs dogs, and the hippocampus
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How does Ca+2 cause short term depression?
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Ca+2 accumulation activates the k channels and inactivates the Ca+2 channels in negative feedback loops.
Ca+2 can do so directly or indirectly: directly landing on the K+ site or acting through calmodulin to both activate the K+ channels, which in turn causes hyper polarization that reduces Ca+2 influx when the AP arrives. No Ca+2 to open Ca+2 channels shows negative feedback of Ca+2 inhibiting Ca+2 |
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Ca+2 can both inhibit/depression and enhance short term synaptic strength. What is the difference
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The amount of Ca+2:Enhancement occurs because Ca+2 cna induce more NT release, and activate Protein Kinase that allows more NT vescicles to add to the releasable NT vescicle stock pile.
Depression: Can inhibit itself by binding to K+ channels (directly/indirectly) and this will cause a hyperpolarization reducing Ca+2 influx and there for reducing the Ca+2 concentration that is required to open Ca+2 channels. |
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The withdrawl reflex in Aplysia californica is an example of what?
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Nonassociative learning.
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What is the difference between habituation and sensitzation?
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Habituation is a form a short term synaptic depression caused by vescicle depletion
Sensitization is an increased in reflex strength and thus faster response than normal |
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If I touch a siphon on the aplysia californica and it withdrawls, and I repeat this over and over and it's response becomes slow this is an example of...
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Vescicle depletion or Habituation
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When I shock a lil slug and it's response is much faster and stronger this is an example of... how long does it last...
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sensitization and can last about an hour
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If I touched a lil slug and shocked it, then it reacts to my touch as if i Shocked it, producing a strong reflex what type of learning would be here?
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Associative learning
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The example of the sea hare where it recoils in response to touch is an example of..
(short term sensitization) |
non associative learning short term sensitization of the gill withdrawl reflex.
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Describe the path way of signal conductance to through the sea slug's gill reflex withdrawal when touched on it's siphon.
(short term sensitization) |
The siphon sensory neuron sends impulses to both the Gill moto neuron and to an interneuron that in turn sends impulses to the gill motor neuron enhancing the effect.
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Describe the pathway of signal conductance of a sea hare when shocked on the tail
(short term sensitization) |
The sea hare's tail sensory neuron goes along a poly synaptic pathway that in turn triggers the facilitatory interneuron that makes synapses with PRE SYNAPTIC terminals of the interneuron and motorneuron.
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When the sea hares tail is shocked and the facilitory interneuron is activated what happens to the AP and potentiation?
(short term sensitization) |
The width of the AP is larger so the AP lasts longer more time when the Voltage gated Ca+2 channels are open.
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When the facultative interneuron synapses to the presynaptic cells it releases which NT?
(short term sensitization) |
5ht or seratonin
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in short term sensitization when the facultative interneuron synapses to the presynaptic cells it causes the sypanse to increase in strength how does it do this? And what is the pathway?
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The seratonin binds to metaba-trophic receptors that activate protein kinases A&C that send reserve vesicles into release vesicle pool.
The pathway is metabatropic receptors activate g-protein coupled ones that lead to activation of Adenylyl cyclase > CAMP> protein Cyclase A that Phosphorylates K+channels> K+ channels more active allow more K+ in and that causes reploarization, and the K+ cant respond to voltage channels. The AP is longer and wider as a result. |
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With the Sea Hare repeated tail shocks, can result in LONG TERM sensitization of the gill withdrawal reflex. How does this occur?
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Repetitive seratonin release can cause some of the active catalytic subunit of PKA makes its way to the cell body, where it enters the nucleaus and phosphorylates the Creb which causes gene transcription.
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An example of where g-protein coupled receptors can have multiple targets in the postsynaptic cells. In the facilitory presyanaptic terminal activation of seratonin receptors by seratonin
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Where PKA can phosphorylate K+ channels and make them more active to increase the width of an AP (lasting longer) where it can cause reserve vescicles to be taken into releasable vescicles,
or when it makes its way to the nucleaus (long term) and causes gene transcription |
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During short term sensitization of the sea hare if you repeatedly touch it, and then shock it will conditioning occur?
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yes as long as the interval between touching and shocking is not too long
CS>US |
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During short term sensitization of the sea hare if you shock the sea hares tail repeatedly then touch it will conditioning occur?
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NO CS -> US for conditioning not vice versa or any time elapsed
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Hippocampus=
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sea horse
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where is the hippocampus located in the brain?
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most medial/inferior part of the temporal lobe
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Describe the hippocampus circuitry
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From Higher cortical levels>parahippocamplan and rhinal cortical areas> hippocampus> fornix>thalmus/hypothalmus
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What is the rhinal cortical area?
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It recieves multi modal sensory inputs from higher level sensory cortical regions
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What is the major output of the hippocampus? and what does it do?
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The fornix, that projects to the neurons of mamillary nucleas of the hypothalmus
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HM couldn't remember squat, but what could he do?
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Mirror drawing, motor skills, procedural memory.
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2 major parts of Hippocampus
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Dentate gyrus, and cornu ammonis fields (Ammons horns)
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Rats hippocampus vs humans hippocampus:
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Rats Located at the ventromedial edge of neocortex that is more posterior than in humans However the circuitry is identical.
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The hippocampus 3 pathways cause LTP that is::
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It can last hours to weeks, (or longer) it is a form of associative learning, it is important for storing long term memories.
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What is the important NT used in the Hippocampus pathways?
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Glutamate
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What are the 3 pathways in the hippocampus (synaptic pathways) that can cause LTP due to high frequency bursts?
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CA1 - CA3 (schaffers collaterals) and the perforant path.
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Axons from neurons in entorhinal cortex enter the hippocampus via a fiber tract, the ________
a. schaffer collaterals b. ventromedial edge c. Ca1 to fornix d. perforant path |
d perforant path
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When high frequency firing in one input is paried with activity of another input how do the inactive inputs become potentiated?
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They don't cakes a lie!
The paired inputs become potentiated however inactive inputs do not. |
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What is required for any of the 3 synaptic pathwyas in the hippocampus to enhance subsequent synaptic responses of the same pathway?
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High frequency AP bursts of about 50-100 AP at 100/sec
to trigger a large depolarization. However even without the 50-100 burst if there is a large depolarization artificially induced one will see LTP |
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What is the significance of not firing the 50-100 AP /sec and still eliciting the presynaptic input that triggers LTP artifically?
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It shows that it's not the 50-100AP /sec that is importance but the release of Glutamate that makes a strong depolarization of the post synaptic cell that is important
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The problem of post synaptic depolarization that depolarizes an entire cell is resolved by which two things?
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The fact that glutamte receptors must lso be activated during the strong depolarization
The structure of glutamate receptors being that of dendritic spines |
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How does the structure of dendritic spines specificy localization of only synapses that were active during LTP of inputs that are fired together.
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The potentiation is restricted to only synapses that were active due to the "Neck of the dendritic spine, it is narrow and isolate NT from diffusion acting as a diffusion barrier.
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How does glutamate trigger LTP during postsynaptic depolarization at specific active synapses?
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The synapses that fired will have glutamate receptors activated that allow calcium influx necessary to trigger LTP.
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What are the two types of glutamate receptors that are in the hippocampal spines?
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AMPA and NMDA
AMPA permeable to Na+ and K+ while NMDA requires depolarization to kick out the Mg+ so that it can be permeable to Na+ K+ and Ca+2 |
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How does Mg2+ react with respect to NMDA
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It blocks the channel as long as the cell is near resting membrane potential. When the cell is repolarized some of the Mg2+ gets kicked off allowing Na+ K+ and Ca+2 to enter causing depolarization
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The experiement that showed yellow and grey dendritic spines was to show that....
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Ony specific receptors where glutamate is released and they in turn caused depolarization so that the Ca+2 influx would cause them to become yellow.
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How does Ca+2 trigger LTP?
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It has two effects on AMPA receptors, and does so through PKC and CaMKII.
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How does the density of AMPA receptors increase due to Ca+2 influx?
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Ca+2 triggers Kinases that phosphoralates AMPA receptors making them more active. And it activates CaMKII that causes new AMPA receptors to be inserted into the membrane.
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What is Long term depression
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It is the opposite of LTP: when synaptic input on a hippocampal neuron is activated at a low rate for a few minutes without strong activity in other synapses.
Weakly stimulated input is reduced because there is no strong stimulus of any other inputs.. :( its a loner |
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What is Ca+2 role in LTD and LTP?
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The amount of Ca+2 determines LTP or LTD, less than 5 um then protein kinases will be released and that will cause phospharylation of synaptic protiens that cause LTP
if there is low u uM protein phsophatase causes Unphosphoralation to synaptic protiens and causes LTD |
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What determines how much calcium is released and ultimately determiens LTP and LTD?
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The frequency is high or low stimulus.
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What is phosphatase?
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It unphosphralizes AMPA's and causes decreased in activity and results in LTD
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What is PSD-95
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something that holds eggs...
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