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What are the differences between short lasting LTP (S-LTP or early LTP) and long lasting LTP (L-LTP or late LTP)?
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Early LTP is induced by weak high-frequency stimulation and is caused by post-translational modifications (e.g. AMPA receptor trafficking). Late LTP is induced by strong high-frequency stimulation and involves new protein synthesis.
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What is the difference between transcription, translation, and post-translation?
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Transcription: creating new mRNAs from DNA
Translation: ribosomes read the mRNAs and form a polypeptide chain that folds into proteins Post-translation: modifications that occur after the protein is made (e.g. phosphorylation, ubiquitination, methylation) |
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Describe the genomic signaling hypothesis.
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Synaptic activity from the high-frequency stimulation will activate signaling molecules that move to the nucleus and phosphorylate transcription factors (CREB), resulting in new protein synthesis.
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What is a transcription factor?
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TFs are proteins that bind to specific sequences in DNA and control the rate of transcription.
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What is CREB? How is it activated?
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CREB stands for cAMP Response Element Binding protein. It is activated by phosphorylation and binds to the CRE sequence of DNA.
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Why do we believe CREB is involved in L-LTP?
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If you knock out or inhibit CREB (or its phosphorylation), you don't get L-LTP.
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What is the difference between synapse-to-nucleus and soma-to-nucleus signaling?
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Synapse to Nucleus: mediated by synaptic activity
Soma to Nucleus: mediated by action potentials |
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How can synaptic activity signal the nucleus to generate new plasticity products?
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 See pic (too lazy to type out) |
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Describe the Dudek and Fields experiment that supports the soma-to-nucleus hypothesis? Why might it also be considered an example of synaptic tagging?
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 Weak Stimulation alone itsn't not enough to induce L-LTP, but weak stimulation plus antidromic stimulation (action potential in axon), will induce L-LTP |
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Why do we believe that L-LTP depends on protein synthesis?
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Add a translation inhibitor (anisomycin or emetine) and block L-LTP
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What basic evidence supports the idea that E-LTP has different molecular requirements than L-LTP?
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Adding actinomycin-D (general transcription inhibitor) before stimulus that can induce LTP will block the long-lasting component but not the short one.
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What is local or dendritic protein synthesis?
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Free-floating mRNAs already in vicinity of dendrites are translated.
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Defend or reject the following statement: In principle, it is possible that synaptic activity could generate two distinct waves of protein synthesis that could contribute to the support of long-lasting LTP.
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There can be a wave of protein synthesis at the dendrite that occurs earlier before genomic signalling ushers in another wave.
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Describe the Kang and Shuman experiment and how it illustrates the role of local protein synthesis.
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 1. Separate dendrites from soma 2. Stimulate Schaffer Collaterals 3. Can still be L-LTP 4. Proteins translated locally in dendrite |
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Briefly describe how Bradshaw et al. reached the conclusion that protein synthesis occurs in dendrites.
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Added emetine to:
Apical dendrites = only block L-LTP @ apical dendrites Basal dendrites = only block L-LTP @ basal dendrites Soma = didn't block L-LTP |
