Lecture 12

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Cell and Systems Biology
Melanie Woodin

CSB332H1S L12; Feb.27, 2012  Bliss & Lomo – late 1960s Synaptic Plasticity  LTP in hippocampus of anesthetized rabbit Read Ch. 16  Blue dots – control, testing strength of synapse o Stimulate perforant fibres every 5min, then record from Look at HM’s brain! principle cell  http://thebrainobservatory.ucsd.edu/hmblog/  Don’t have to look at o See strength stays same – so sees test stimulus doesn’t change  Died a few years ago, brain preserved synapse strength, so get baseline o During test stimulation, test EPSP not enough to open AMPAR  Red dots are stimulated pathway, trying to induce plasticity at arrows o Tetanic stimuli (15/s for 10 sec) to PP at arrows  Tetanic = 100Hz or more (100 or more atc pots per sec, high freq) o Record from granule cells in DG o Amplitude increased by 175%, keeps increasing, lasts for hours o Depolarization enough to remove Mg block  Ca influx  more AMPARs in membrane  greater response o So testing AMPAR response  Q: Global response in neurons, or only changes at those presynaptic inputs? o LTP: Specific to input stimulated, need for learning & memory  There are other types of long-term plasticity but LTP & LTD are the 2 most studied  Rat hippocampal slice  Intracellular recording from postsynaptic CA1 pyramidal cell  Need to lay down long term memories o Not normalized, shown in mV  Laminant structures – well identified  Stimulating electrodes in 2 distinct grps of presynaptic fibres in SC pathway (don’t cross paths)  Pathways w bundles of axons, cell bodies in thal  Control: Amplitude increases but goes down within minutes   Act pots down bundle of axons (Perforant fibre pathway) onto dendrities of principle neurons in Dentate gyrus  If stimulate one on own, don’t get LTP   release glutamate  AMPA & NMDA (excitatory synapses) o But if stimulate both inputs together  can induce LTP o Cooperate/associate to produce potentiation by stimulating at   summate at cell bodies in Dentate same time   axons synapse onto dendrites in principal cells in CA3  Associative LTP – repetitive activity to one synaptic input to a cell can   excitatory synapses, if enough then generate act pot to Schaffer influence whether another input to the same cell is also potentiated Collateral (SC)   synapse on pyramidal cells (principle cells) in CA1 by repetitive activity o Goal is to remove Mg block   axons leave hippocampus thru Subiculum  thal, cortex o Depolarization spreads to neighbouring regions  associates/summates  Dendritic spines prob used to make sure only certain AMPARs affected  specificity NMDA & AMPA receptors o Activated of Calmodulin  phosphorylation of CaM Kinase II   Glutamate = major excitatory neurotransmitter of CNS can stay active well past time of Ca signal (Ca quickly chelated)  Glutamate binds to NMDARs & AMPARs postsynaptically  CaM Kinase II: o Binds to other as well o Strengthens synapse: phosphorylates AMPARs at membrane  o Most located postsynaptically incre
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