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Thread: Long Term Potentiation and Memory

  1. #1 Long Term Potentiation and Memory 
    Forum Freshman thirdeye's Avatar
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    Hi all,

    So I was reading about memory and the brain, and stumbled on a thing called "long term potentiation." I couldn't really grasp what the book was trying to get across, but I could manage to understand that it has to do with presynaptic and postsynaptic responses of a neuron. Is it basically the strengthening of these responses/reactions?

    Also, it was described that LTP is similar to the process of long-term memory. How is this possible exactly? Does this have to do with the "memory" of a neuron?


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  3. #2  
    墨子 DaBOB's Avatar
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    Well, since no one else has replied I'll do my best.

    I'm not sure this is what your talking about but here goes: As you age neurons die and connections are made more permanent.

    Think about it like a massive maze of highways. You build a large city with new stuff everywhere and individual roads that go to each place. As time goes on certain roads aren't used and certain shops aren't needed so to speed things up they are demolished and faster roads are put in.

    As connections become stronger and neural tissue is lost the brain becomes more efficient.

    Is that what your talking about, or am I way off?


    Do not try and bend the spoon. That's impossible. Instead... only realize the truth. There is no spoon. Then you'll see that it is not the spoon that bends, it is only yourself. -Spoon Boy
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  4. #3  
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    I don't really know everything about it, but I had to learn this last year.
    Long term potentiation has to do with making postsynaptic cells more sensitive to glutamate.

    Normally, glutamate goes from the presynaptic cell via the synaps to glutamate-receptors (AMPA receptors) on the postsynaptic cell. Glutamate binding to the AMPA receptor triggers the influx of predominantly sodium ions into the postsynaptic cell, causing a depolarization called the excitatory postsynaptic potential (EPSP). But there are also other glutamate-receptors, e.g. NMDA receptors. These are normally blocked by a Mg-ion that binds to the inside of the NMDA receptor channel (when opened by glutamate-binding) before any other ion can enter the channel. This Mg-ion is voltage-dependent. In other words, when the postsynaptic cell becomes depolarized, the Mg-ion will let go of the NMDAR channel, and Ca-ions will pass through the channel inside of the postsynaptic cell. This depolarization of the postsynaptic cell will only occur after the summation of the EPSP's will reach a certain level (about -10 mV I think).

    After these Ca ions enter the postsynaptic cell, in some way (and here it gets a little hazy) they mediate the insertion of other AMPA-receptors in the postsynaptic cell, making the postsynaptic cell more sensitive to a small amount of glutamate, making it easier for the postsynaptic cell to reach the requiered action potential with an EPSP.

    I hope this clarifies a bit more, sorry for the lacking English, but it's difficult explaining something in a language different than your mother tongue (that, and I'm tired )
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