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23 Cards in this Set
- Front
- Back
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Where are Engrams found? |
association areas that get sensory input from primary sensory areas |
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Where does association area send sensory info? |
sends the sensory info to medial temporal lobes for processing in the hippocampal formation which then sends it back to associated areas for consolidation |
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What kind of memories are in the prefrontal region? |
working memory and stored info about source to relate memories to time/place |
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What's the hippo-formation comprised of? |
dentate gyrus, hippocampus & subiculum |
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What's the pathway to make declarative memories |
sensory info >> cortical association areas >> parahippo & rhinal cortical regions >> dentate >> hippo >> subiculum >> fornix >> hypothal >> thal ***SUBICULUM ALSO SENDS BACK TO CORTICAL ASSOCIATION AREA!*** |
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What's the steps to the hippo pathway? |
Sensory Stim >> Entorhinal cortex >> Perforant Pathway >> Dentate >> CA3 pyramid cells >> Fornix (dead end) and Schaffer collaterals >> CA1 pyramids >> subiculum >> Back to Entorhinal cortex |
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What's the importance of the hippo pathway? |
This pathway generates SYNAPTIC PLASTICITY |
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Where does LTP take place? |
In hippocampus (and elsewhere) |
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How does LTP develop? |
HFS (100/s) to CA1 from CA3/Schaffer collaterals ==> increases synaptic efficiency = LTP (the CA1 is GLUTAMINERGIC) |
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Early & Late changes in CA1 during LTP formation that promote LTP formation |
Early = increased sensitivity to glutamate dt AMPA receptors popping up on dendritic spines --> Late = More synapses between CA3 & CA1 -----> both of these changes make CA1 more likely to be excited by CA3 |
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What NT promotes LTP & how does it work? |
Glutamate --> binds to AMPA & NMDA --> AMP cation channels open and let Na enter = EPSP ---> but NMDA channels blocked by Mg |
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what does temporal summation of CA1 do? |
Prolongs and enlarges the depolarization and removes Mg out of channels to let Ca enter --> more Ca = activation of PKC & CAMK-2 (calc-calmod-dependent protein kinase 2) |
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LTP formation requires what 3 elements? |
High AMPA channel conductance (early event), High # AMPA receptors (early event), & High # synapses (late event) |
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What happens when it's low frequency instead of high frequency stimulation of CA1? |
LFS = 1/s = Excitatory synapse loses efficiency ==> LTD!!! |
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What is the pre-req for LTP/LTD? |
Both require activation of NMDA receptors |
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What's the difference between HFS & LFS? What are the end results? |
HFS = >5pM Ca = activation of both kinases that phosphorylate key proteins for LTP --> LFS = <1mM = activates protein phosphatases that cause for AMPA receptors to get internalized & lower CA1 sensitivity to glutamate = LTD (and less EPSP magnitude) |
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What other types of cells use this mechanism of LTP/LTD? |
Layer 3 of inferotemporal cortex --> cells here respond to those in layer 4 in a frequency-dependent way like CA1/CA3 |
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What sites are involved in non-declarative memory? |
Motor cortex (supplementary & pre-motor), Striatum (BG), and Cerebellum |
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What/where are purkinje cells and where do they get their input from? |
These are the only output cells of the cerebellum = get 2x excitement = single Parallel fiber in outer/molecular layer and Climbing fiber with many synapses |
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What do climbing fibers do to Purkinje cells? |
Releases an excitatory NT that opens Na channels --> after depolarization the Voltage-Sensitive Ca-channels in dendritic membrane open up |
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What does parallel fibers do to purkinje cells? |
Releases glutamate that binds to AMPA and to metabotropic receptor in dendrite |
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What 3x are required for LTD in pukinjes? |
1) more Ca dt climbing fiber stimulation, 2) More sodium dt AMPA channel opening, and 3) activation of protein kinase C dt glutamate metabotropic receptor activation |
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What happens when there's LTD in purkinjes? |
It induces the phosphorylation of AMPAs >> they get internalized >> lowers sensitivity of dendrites to glutamate released by the parallels |
