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How is neurotransmitter released from a receptor?

  1. Apr 7, 2010 #1
    What makes it release back into the synpatic cleft? Also in other scenarios I have seen some ligand or something attaches to a receptor and then get released without any mention why it happened? If anyone can help. It would be great. Thanks :smile:
     
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  3. Apr 7, 2010 #2

    Ygggdrasil

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    All non-covalent binding reactions are reversible. Typically, binding occurs through a variety of weak intermolecular forces (e.g hydrogen bonds, van der Waals interactions, hydrophobic effect) whose strength is on the order of the thermal energy of the system. Therefore, thermal fluctuations of the receptor and/or ligand can break the bonds between receptor and ligand, releasing the ligand back into the synaptic cleft.
     
  4. Apr 7, 2010 #3
    Thanks Ygggdrasil your replies are never dissapointing :smile: I have one question though. Let's say neurotransmitter open sodium channels and sodium comes into the cell, then there would be less sodium in the side where the neurotransmitter is attached to the receptor, then there is less heat there and get it released (but less heat doesn't break bonds right?). Can you give your opinion on this. Thank you!!
     
    Last edited: Apr 7, 2010
  5. Apr 8, 2010 #4

    Ygggdrasil

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    1) There is a large volume of liquid in the extracellular space that contains a lot of sodium. I dont' think opening sodium channels alters the sodium concentration that much (although I'm not 100% sure and could be wrong about this).

    2) Why would you expect opening sodium channels to decrease the temperature of the extracellular medium?
     
  6. Apr 8, 2010 #5
    I just want to know how the receptor for example releases the neurotransmitter at the right time. If it is atttached forever sodium would continue to come in, can you give me an example of thermal fluctuation that releases a ligand or neurotransmitter from a receptor? I just want to know if it is random how does it release it at the right time. Thanks!!
     
  7. Apr 8, 2010 #6

    Ygggdrasil

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    The release occurs randomly. One can perform single channel recordings to look at individual channel opening and closing events. From these experiments, you can look at the amount of time between when the channel opens to when it closes. This would correspond to the lifetime of the receptor-ligand interaction. Looking at many binding events, you should find that he distribution of binding lifetimes follows an exponential distribution, indicating that the dissociation process is stochastic.

    The time constant for the dissociation process depends on the size of the thermal fluctuation (i.e. the activation energy) needed to disrupt the receptor-ligand interactions.
     
  8. Apr 8, 2010 #7
    Thanks again for help :smile: I'm assuming that these bonds are vey weak and last less than the length of an action potential or else there would be reoccurence of that.
     
  9. Apr 8, 2010 #8

    Ygggdrasil

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    Probably, although I don't know the numbers off the top of my head. Also remember that the opening of voltage-gated potassium channels and subsequent hyperpolarization of the neurons after an action potential lead to a refractory period during which another action potential cannot occur.
     
  10. Apr 19, 2010 #9
    Neurotransmitters are usually stored in vesicles in the pre-synaptic neuron and are released into the synapse in response to an action potential. How does an action potential cause neurotransmitter release? During depolarization of the pre-synaptic terminal, voltage-gated calcium channels open and allow calcium ions to flow into the pre-synaptic terminal. Vesicles filled with neurotransmitters are docked on the cytosolic side of the plasma membrane and are coated with proteins called SNAREs. Basically, these proteins fuse the vesicles with the membrane when calcium is present, which causes neurotransmitters in the vesicles to be pushed into the synapse. Neurons can even store vesicles with different neurotransmitters which are coated in different proteins which require a higher frequency of action potentials to induce exocytosis. So a low frequency of action potentials might only lead to glutamate release, but a higher frequency of action potentials may cause a higher pre-synaptic calcium influx leading to dopamine or serotonin release.

    http://en.wikipedia.org/wiki/SNARE_(protein)
    There's a nice picture in the SNARE topic in wiki that gives an idea how these proteins mediate vesicle fusion through calcium binding.
     
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