B&NG2

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steena_k
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139046
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B&NG2
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2012-03-05 23:19:26
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EXAM
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EXAM 2
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  1. What is the general function of protein kinases?
    They phosphorylate proteins and enzymes to activate pathways.
  2. What is the general function of protein phosphatases?
    They dephosphorylate proteins and enzymes to deactivate pathways.
  3. Name at least 5 protein kinases known to be involved in memory.
    • CaMKII
    • 5-HT
    • PKA
    • NR4A
    • CREB
  4. Name 3 events that activate CaMKII.
    • 1) Calcium influx
    • 2)self-phosphorylation
    • 3)CaMKII calmodulin kinase II
  5. What are the main conclusions of the Alcino Silva and Susumu Tonegawa t wo papers in Science in 1992? What experiments were performed to show that α‐CaMKII is lacking in the α‐CaMKII mutant mice?
    Neuronal alphaCaMKII become known as a memory molecule and mice lacking this molecule became deficient in long term potentiation and spatial learning. To show that alpha camkII was lacking by giving a schematic representation of the construct used for the targeting experiement and compared wt mice to KO mice (Sections with alpha CAMKII) in Southern and Western blotting. They also showed the wt brain and the KO brain to show nothing else was affected.
  6. What does it tell you if a gene knockout leads to deficits in hippocampal LTP and context fear memory?
    That the gene is important in LTP and context fear memory and that no other gene took over it's function.
  7. Why PKMζ is different from many other molecules involved in memory?
    It's involved in storage of the memory (and encoding) not acquisition like all the other molecules we study and know about.
  8. Which molecules does PKMζ help to keep at the synapse?
    AMPA receptors.
  9. Why PKMζ is important?
    It's important to learn more about the memory process (especially acquisition since not as much is known).
  10. Explain dependence of long‐term memory on protein synthesis.
    If you inject a protein synthesis inhibitor and train then test the mice you find out that long term memory is deficient but not short term memory.
  11. What is synaptic trafficking?
    In synaptic trafficking PKMzeta once it is synthesized binds to and is phosphorylated by PDK1 which increases the activity of PKMzeta. PKMzeta potentiates AMPA-R increasing the number of receptors in the post synaptic density through the action of the trafficking protein NSF.
  12. Describe how phosphorylation can activate or inhibit signaling pathways.
    phosphorylation can activate many enzymes and molecules that will bind to or go on to phosphorylate other molecules in that pathway, by a phosphorylation the pathway can be signaled ON and take place. (some molecules undergo conformational change through phosphorylation which activate a pathway). With the activation of the signal the protein or enzyme is phosphorylated and the pathway continues.

    In ubiquitination phosphorylation inhibits the pathway, turning it off.
  13. What is constitutive or persistent activity?
  14. Describe AMPA‐R endocytosis.
    The starting signal for AMPAR endocytosis is an NMDAR-dependent calcium influx from low-frequency stimulation, which in turn activates protein phosphatases PP1 and calcineurin. However, AMPAR endocytosis has also been activated by voltage-dependent calcium channels, suggesting general calcium influx as the cause of AMPAR endocytosis

    expect memory to be lost.
  15. Describe AMPA-R trafficking.
    In synaptic trafficking PKMzeta once it is synthesized binds to and is phosphorylated by PDK1 which increases the activity of PKMzeta. PKMzeta potentiates AMPA-R increasing the number of receptors in the post synaptic density through the action of the trafficking protein NSF.

    This can activate a "silent synapse".
  16. Describe protein synthesis at the synapse.
    In neurons, an internal promoter produces PKMz mRNA that is translationally expressed. Once synthesized PKMz binds to and is phosphorylated to PDK1 which removes the translational block and increases PKMz acticity.
  17. Explain the process and effect of increased number of AMPA‐R at the PSD potentiate synaptic transmission.
    PKMz potentiates AMPAR responses by increasing the number of receptors in the postsynaptic density through action of the trafficking protein NSF.
  18. What is a silent synapse?
    An excitatory glutamergic synapse whose postsynaptic membrane contains NMDA type glutamate receptors but no AMPA type receptors so it is inactive.
  19. how is AMPA‐R phosphorylation and presence at thesynapse is correlated with LTP/memory?
    When ampa-R are phosphorylated by CaMKII this triggers more becoming inserted in the post synaptic synapse and increase LTP and enhance memory (postsynaptic responses are enhanced).
  20. how is AMPA-R phosphorylation and presence at the synapse correlated with LTD/forgetting?
    AMPARs are diminished in the synapse. PKMzeta binds to a substrate that decreases AMPAR endocytosis. after LTD induction, AMPARs are removed.

    • can occur from persistent weak stimulation.
    • less phosphorylation of AMPAR
  21. Describe spaced and massed training and their similarities/differences.
    Spaced training is an effective way to produce skills because it allows forrepetition over time. Builds up long term potentiation. More consolidation time.

    massed training which tries to cram training into one or two sessions. Massed training is a far less effective strategy for retaining knowledge or developing skills.
  22. how do we visualize activated neurons ?
    • mice must be dead
    • Cre-LocZ mouse. Cre phosphorylates.
    • activated neurons will end up blue.
    • Cre binds creb and we know that creb is for memory.
  23. Describe Cued fear conditioning.
    In cued fear conditioning a mouse is placed in a box (that it has habituated to) and then a neutral tone is played, during the tone the mouse is shocked.After a few trials the mouse should learn to anticipate theshock from the tone (freezing). They are tested about 24hrs later and freeze at the sound of the tone.
  24. Describe context fear conditioning.
    First a mouse is exposed to a new context (not the homecage). Once it's habituated it then receives a shock. It's tested 24hrs later in the same context (should display freezing inside the same context).
  25. What are the anatomic regions involved in learned fear (for each kind of learned fear)?
    • CUED- DIRECT: tone, Auditory thalamus to the Amygdala (Lateral nucleus to Central Amygdala) and then response.
    • INDIRECT: tone, Auditory thalamus, auditory cortex, amydala (lateral nucleus, Central) then the response.

    CONTEXT: Visual subiculum, contextual stimulus, Basolateral and accesory basal of amygdala to central amygdala to the respose.
  26. why are genes expressed selectively in brain areas important to find?
    genes expressed selectively in the brain may be specified for particular behaviors and you can find a reason fr selective expression. Can make a KO to study what is effected (test function in the brain).
  27. Name different types of neurons and their markers.
    excitatory/pyramidal neurons- Glutamate -> camKII alpha is the marker

    inhibitory/interneurons- GABA-> GAD is a marker and GABA
  28. describe the process of how cDNA library made.
    • 1. cut area of brain (amygdala)
    • 2. separate cells with enzyme (proteinase)
    • 3. place each cell in separate tube with lysis buffer -> rna will be exposed
    • 4. make cDNA using reverse transcriptase from retrovirus
    • 5. destroy other rna with rnase H and it will become double stranded.
    • 6.amplify with PCR
    • 7. make cDNA library- package product into bacteriophage
  29. how amygdala and hippocampal probes for differential screenings are made?
    • 1. make a radioactive probe for hybridization from rna ->pcr-> amygdala probe OR bacteriophage to RNA probe and view contrast of expression to differentiate (when placing cDNA from library on agarose plate bacteria will cover and holes will form).
    • 2.stronger spots = stronger expression
  30. Brain Regions and Neural Circuits.
  31. What memory problem did patient H.M. have? How was memory affected?
    He was having seizures after an accident so they removed parts of his some parts amygdala and hippocampus (bilateral). He kept his old memories but couldn't form new ones (except for skilled memories but didn't remember ever learning them).

    The first and the best-studied case of the effects on memory of bilateral removal of portions of the temporal lobes was the patient called H.M.• H.M. was unable to transfer new short-term memory into long-term memory, but he had good recollection of the past events
  32. Define and describe implicit memory.
    • priming, skills and habits and associative and nondissociative memories.
    • neocortex, striatum, amygdala, cerebellum, reflexes.
  33. Define and describe explicit memory.
    • Facts and events.
    • Medial temporal lobe
  34. Provide a detailed diagram with explanations of the cAMP‐PKA‐CREB pathway
    • Ca2+ influx activates NMDA receptors which activate CaMP. cAMP binds to the 2 regulatory subunits of PKA (Stay in the cytoplasm).
    • the 2 catalytic subunits of PKA go to the nucleus to phosphorylate CREB (transcription factor).

    this pathway turns on the genes involved in stabilization of memory.
  35. Name protein kinases thatdirectly activate CREB.
    • CaM Kinases: CaMP Kinase.
    • cre
  36. Describe the Dominant‐negative approach.
    • Dominant mutations in which the product of the mutant allele interferes with the function of the normal allele in the heterozygous state.
    • A mutation whose gene product adversely affects the normal, wild-type gene product within the same cell. This usually occurs if the product can still interact with the same elements e the wild-type product but block some aspect of its function product.

    DN is inhibitor that leads to lack of function (post translational interference), Binding is normal but you can't phosphorylate. Can have dominant ligand or receptor.

    • functional knockout (not a real knockout)
    • Get 50% Aa, 25% aa, 25% AA

    PKA R-subunit is usedto create a dominantnegative mutant
  37. Name the Brain regions involved in different types of fear memory.
    prefrontal cortex, hippocampus, basolateral amygdala, central amygdala
  38. What is reconsolidation and fear memory extinction?
    extinction- context dependent. weakends CR to CS. Inhibits original memory but it still exists/ Medial prefrontal cortex invovled heavily.

    reconsolidation- uses more of the amygdala. ability to retrieve/ move from/into long term memory.
  39. How can amygdala regulate other types of memory?
    Emotional dependent memories are regulated by the hippocampus.
  40. Why is it interesting/important to study fear memory?
    We know the neural circuitry of fear processing so you can study the function of the genes and ultimately combine function and anatomy into one good model.

    Learned fear is the best available model in acquired mental illnesses (stage fright, PTSD, Panic attacks, autism).

    Amygdala is the brain structure where the causal relationship between LTP and behavior is shown most convincingly.
  41. Name two genes involved in fear memory.
    • GRPR involved in fear memory inhibition. (KO mice show enhanced memori in cued and fear conditioning. They have less GABA released and less inhibition than normal wt mice.)
    • Stathmin invovled in fear memory enhancement. (expressed in BLA stathmin deficient mice have deficits in innate fear and cued and contextual fear conditioning but normal spatial memory)/

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