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Medical Action Potentials

  1. Dec 23, 2005 #1
    1. How does an Action potential start in the nerve. Does it just recieve a stimulus and suddenly the inside of the nerve depolarizes??:confused: How does the inside of the nerve become more positive??

    2. In people with Multiple Sclerosis the myelin on the nerve is broken down & the AP doesn't tavel down the nerve..Why cant the AP move down the nerve just like it does when the myelin is there? How does the AP tavel down a myelinated nerve? I know there is no Na/K voltagate gated channels where the myelin used to be so how does it travel?


    Thanks
     
    Last edited: Dec 23, 2005
  2. jcsd
  3. Dec 23, 2005 #2
    ANOTHER QUESTION: I read that "because of the absolute refractory period of the Na+ voltage-gated channels, two action potentials cannot be fired one on top of the other. Therefore, action potentials will almost always have a fixed height or amplitude"

    Can't an action potential be fired because before the Na+ voltage-gated channel (the one in refactory period) there is a Na+ voltage-gated channel that can be excited right?? Could someone explain how the "potentials will almost always have a fixed height or amplitude"

    Thanks o:)
     
    Last edited: Dec 23, 2005
  4. Dec 26, 2005 #3
    http://www.cyberpunks.org/freeside/mab_neuro.html
    So the way the depolarization travels is pretty much the same way it does in an ummeyelinated neuron: each change in voltage depolarizes the next little bit of length whose voltage then changes. But by insulating a length of axon the change in voltage is instantly shunted much farther down the axon where it acts to depolarize the uninsulated nodes. These then fire and reinforce the change in voltage down to the next node. Saltatory means "jumping". The advantage of this is increased speed. When the myelin is destroyed, in most cases the neuron still fires, but is considerably slower than normal and loses all coordination with other neurons:
    http://serendip.brynmawr.edu/bb/neuro/neuro01/web1/Blumenfeld.html
    I'm not sure why the signal is only slowed in some cases and completely dissipated in others. Perhaps it's just a matter of how many segments of myelin in a row are missing. If only 1 mm is missing then perhaps the signal is merely slowed, but if 3 mm are missing then it completely attenuates. I'm not sure.
     
  5. Dec 26, 2005 #4
    When the right neurotransmitters are recieved they tell the cell wall to open some gates and let the ions that have been pumped outside the cell back into it.
    The opposite of the way it becomes "less positive". It becomes less positive when the pumps push more ions out than are coming in. Like charges repell. Positive repells positive. All these positive ions want to spread themselves from each other evenly and won't concentrate anywhere on their own. Pumps have to physically push them from the inside of the cell to the outside where they are more crowded. The outside of the cell is then more positive with respect to the inside, and given the chance the ions will automatically spread back into the inside of the neuron where there is less pressure. When the first gates in the cell wall open and let ions in the next gates in line sense this increase in positive charge inside the cell and they automatically open to let more ions in.

    A given neuron may get 20 different neurotransmitter messages before it fires. Some neurons give it the message "don't fire" and others give it the "go ahead" neurotransmitters. It has to get the right number and kind of "go ahead" signals before it crosses the firing threshold and the first gates open.

    That's all a bit casually put, but I hope it helps.
     
  6. Dec 26, 2005 #5

    somasimple

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    Zoobyshoe,

    this explanation about saltatory condution is the actual and teached one but it remains absolutely illogical and against all the principles I know in Physics.
     
  7. Dec 26, 2005 #6
    Maybe you should start a thread in Mind and Brain about it. Explain what the teaching claims with backup from links and then why you think this violates physics, with links.
     
  8. Dec 27, 2005 #7

    somasimple

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    Zoobyshoe,

    You're right!
    I'll try to make a thread about these riddles/mysteries.
     
  9. Dec 28, 2005 #8
    thank you :biggrin:
     
  10. Dec 29, 2005 #9
    This part of Roxy's question has an intriguing angle to it. Since an action potential has to start with a stimulus, does it mean that there is no such thing as free will?.....i.e. is every neuronal activity a response to some sensory stimulus? Makes me wonder....
     
  11. Dec 29, 2005 #10

    selfAdjoint

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    Question, is free will even a testable scientific concept?
     
  12. Dec 30, 2005 #11

    somasimple

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    Hi All,

    B]Free will[/B] is a questionnable scientific question!
    And there is, of course, stimuli that bring neurons to create action potentials.
    It may be answered with some logical and known theories/physics laws => Newton, Gauss, Coulomb...
     
  13. Dec 30, 2005 #12

    selfAdjoint

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    Benjamin Libet did an experiment that shows your brain "knows" what you're going to do around half a second before you decide to do it. Libet tried manfully to square this fact with free will, but most people don't think he managed to bring it off.
     
  14. Jan 1, 2006 #13
    At the outset, I apologise for my cavalier usage of the term 'free will'. Of course, I never meant to use the term as some phenomenon that went beyond physics! But the usage is unpardonable nonetheless.
    What I actually wondered was whether there exists a mechanism other than sensory stimuli relayed to the CNS which can elicit an action potential in a neuron. Can the brain begin a train of thought without an external stimulus prompting it onto that line of thought? If it can, how are the first neurons excited? How are the first action potentials initiated? Or are thoughts only elicitable as a consequence (albeit extremely indirect) of sensory stimuli?
    So in essence, I am defining free will here as the ability of the brain to initiate activity independent of sensory input. It does not, of course, mean that I am talking about any activity which is independent of the genetic and epigenetic phenomena that construct the brain and the life experiences that mould it.
     
  15. Jan 1, 2006 #14
    I think that what people experience in sensory deprivation tanks is the best indication that the brain is always self stimulating with a greater or lesser amount of corrective or stimulatory imput from the outside. Once we remove as much sensory imput as possible, the brain continues thought and sensory processes with information from memory. More and more the result is imaginary and eventually hallucinatory: sensory experiences become stimulated by internal stimluli rather than external, while being just as vivid.

    In some point during our first few years of life we shift from constant reaction to outside stimuli to a preference for internal stimuli: we check things against memory, and conduct analyses of outside stimulation with processes, and "values" stored in memory.

    I think the answer to your question is, not only can the brain stimulate itself from within, but that this is what it usually ends up prefering. Learning is essentially the process whereby we stop automatically reacting to external stimuli and modify our reactions increasingly with stored knowledge.
     
  16. Jan 1, 2006 #15
    I do not think that the sensory deprivation tanks truly deprive us of sensory stimuli. The most important reason I can think of is the fact that the photoreceptors have their highest firing rates in darkness! Impinging photons drive down the firing rates. So I would suggest that the thoughts generated during 'sensory deprivation' are influenced by this input from the photoreceptors reporting the darkness that they are 'seeing'.
    As you have yourself pointed out here, we evaluate the external input against our internal representation....so the drive is still sensory.
    I am not disputing the modulatory influences of learning To quote myself....... are thoughts only elicitable as a consequence (albeit extremely indirect) of sensory stimuli? ......and.......It does not, of course, mean that I am talking about any activity which is independent of the genetic and epigenetic phenomena that construct the brain and the life experiences that mould it.
    So all I am wondering is whether there are mechanisms which can begin an action potential in a neuron by itself without the presynaptic neuron being active. (Of course we are not talking about random firing due to leaky channels or other such epileptic phenomenon)
     
  17. Jan 1, 2006 #16
    I don't guess you ever had a question then, but an idea you'd already thought out that you wanted to present.
     
  18. Jan 2, 2006 #17

    somasimple

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    Normally, your asking will bring a firmly negative response since noboby has seen a neuron, firing, without any reason. If it was the case, the system will be crasy.

    But a neuron may be sensitized. It means that many ions channels may be "plugged" in membrane acting again a "threat". Then a neuron, that normally do not react to mechanical stimulation, may fire in such circumstance.
    It is called:allodynia.
     
  19. Jan 2, 2006 #18
    It was neither a question nor an idea. I was just wondering if the mechanism of action potential generation constrains the brain into only reacting to external stimuli and never on its own.
    I am sorry somasimple...i couldn't understand this. Are you talking about potentiation/depression (LTP /LTD)? And I thought allodynia was increased pain sensitivity due to subthreshold injury to the peripheral pain receptors! Please correct me if I am wrong. Thanks
     
  20. Jan 3, 2006 #19

    somasimple

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    Hi,

    I'm lost with this statement since brain is made by neurons and of course they are neurons that are kind of clock/timers that fire continuously and the rate are modified by some other neurons.

    No I'm talking about neurons that are changing of behaviour:

    J Neurophysiol 90: 1949-1955, 2003. First published April 30, 2003; 10.1152/jn.00175.2003
    0022-3077/03
    Inflammation Induces Ectopic Mechanical Sensitivity in Axons of Nociceptors Innervating Deep Tissues
    Geoffrey M. Bove1, Bernard J. Ransil2, Hsi-Chiang Lin1 and Jeong-Gill Leem1
    1 Department of Anesthesia and Critical Care Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215; 2 Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215
    Submitted 25 February 2003; accepted in final form 30 April 2003
    A variety of seemingly diverse pain syndromes are characterized by movement-induced pain radiating in the distribution of a peripheral nerve or nerve root. This could be explained by the induction of ectopic mechanical sensitivity in intact sensory axons. Here we show that inflammation led to mechanical sensitivity of the axons of a subset of mechanically sensitive primary sensory neurons. Dorsal root recordings were made from 194 mechanically sensitive neurons that innervated deep and cutaneous structures and had C, A alpha, and A delta conduction velocities. No axons of any category were mechanically sensitive in control experiments. However, the axons of neurons innervating deep structures and having C- or A delta -conduction velocities became mechanically sensitive during the neuritis, and also exhibited an increased incidence of spontaneous discharge. The incidence of mechanical sensitivity followed a distinct time course. In some cases, paw withdrawal thresholds were obtained after neuritis induction. The time course of the resultant hypersensitivity was not directly related to the time course of the axonal mechanical sensitivity. Ectopic axonal mechanical sensitivity could explain some types of radiating, nerve-related pain coexisting with diseases of seemingly diverse etiologies.

    Address for reprint requests: G. M. Bove, Department of Anesthesia and Critical Care, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Dana 721, Boston, MA 02215 (E-mail: gbove@bidmc.harvard.edu).
     
  21. Jan 3, 2006 #20
    Tonic activity of a neuron is an interesting point that you have raised. But as I thought about it, I realized that even they need an excitatory or an inhibitory input to modulate their firing rates and hence convey information. So, the necessity of the presynaptic activity is not obviated even in this case.

    Thanks for the allodynia reference. :-)
     
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