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Sensory adaptation, how exactly does this occur, also @mtc1973?

  1. Feb 16, 2011 #1
    Hello everyone,

    I read many articles on this, but they all just say what it is and does not mentions how it occurs.

    mtc1973 gave me a good explanation while back, but I have few questions about it.

    1. So if sodium channels go into locked position, does this increase the threshold for the stimulus. Let's say if previous threshold was -20, and then sodium channes got locked in, but threshold should stay the same right, it is just that there is a barrier to reach the previous threshold.
    2. How do sodium channels get locked up, and does this decrease the frequency of action potential or inhibit?
    3. How do we adapt to smell?
    4. For receptor changes I'm assuming, that displacemnet of lamella in pacinian corpuscle reducing pressure as an example.

    Thanks :smile:
  2. jcsd
  3. Feb 16, 2011 #2

    just spend 10 mins typing a reply - to then press a shortcut key to leave the page before posting!!!

    When I can face another 10 mins typing I'll re do it.
  4. Feb 16, 2011 #3
    Until then,
    #1 Threshold potential is the same, but the stimulus will have to be greater to achieve threshold, because there is inhibition.
    #2 Check out the ball and chain model of sodium channels. It is literally a ball and chain domain that acts to block the channel.
    #3 It happens very quickly as I'm sure you have experienced. I think smell is a great example of inhibition, but exactly how at the system/molecular level, I don't know.
    #4 Yo no se hombre.
  5. Feb 16, 2011 #4
    Voltage gated sodium channels have 2 voltage sensitive response elements or gates. Think of a door with a small corridor through the membrane then another door - so 2 doors in series. These doors are called the m gate or activation gate, which is closed at normal resting membrane potential. The other door is the h gate or inactivation gate and it is open at resting membrane potential. But both gates need to be open to allow sodium influx and cell depolarization.
    Threshold is essentially the voltage at which the m gate opens, now both gates are open and we trigger sodium influx and an action potential. However, the h gate is also voltage dependent and closes when the cell depolarizes. Hence we get a transient opening of both doors and an action potential, but it is self limiting because of the closure of the h gate. Here is the important thing, the h gate requires repolarization to reset, otherwise it stays closed and no more action potentials.
    The h gates will remain closed when a cell is depolarized slightly, even sub threshold, especially chronically - like hyperkalemia.
    This leads to no possibility of an action potential. Does this change threshold - no. But that is besides the point really, as no action potentials are possible.
  6. Feb 16, 2011 #5
    So essentiually you can think of 2 thresholds - the threshold of depolarization required to open the m gate and allow an action potential to proceed. And once an action potential has occurred - a threshold that the membrane potential must reach (i.e. a hyperpolarized state) in order to reset the h gate and m gates and allow the next action potential.
    The opening of K channels is what causes that repolarization and allows the h and m gates to reset. Incidentally, whilst the gates are transitioning to the reset level - they obviously cannot sustain an action potential - hence an absolute refractory period.

    These channel kinetics were described back in the 50s by Hodgkin and Huxley before we even knew about single channels and gates. They deduced the whole scheme from the whole cell squid currents they recorded - amazing work that predicted a whole lot about activation and inactivation states - before molecular biology caught up and gave us a mechanism.
  7. Feb 16, 2011 #6
    Thanks both of you for your replies :smile:

    @mtc1973: That is very interesting what you said. So from what I understand i, when there is chronic depolarization, the absolute refractory period is not occuring and there is always depolarization, and no time for gates to reset. Now if I suddenly increase the strength of the stimulus to any depolarized value, does that mean still no action potential, because channels are still in locked position. So only way to respond to the stimulus again is by repolarisation, how can we repolarise it again physically? Also does this mean to have a continuous contraction like muscle, the nerve has to discharge its action potentials with correct timing, so it allows the absolute refractory period to occur, before the next action potential is send. Also definition of adaptation stays frequency of the signal decreases, but from your explanation no action potential is possible, I'm assuming frequency eventually decreases to no action potential state. Thanks :smile:

    EDIT: Also my friends think sensory adaptation involves changing of threshold, I disagree with this. Also what are examples where threshold is increased. I can't think of any.
    Last edited: Feb 16, 2011
  8. Feb 17, 2011 #7
    More detail later,

    but - the threshold can change - based on calcium and other divalent cation levels. A lot more space needs to be put aside to explain that - will have to wait until later.

    As far as the normal situation is concerned however, threshold is the voltage at which the Na channels m gate opens, (notwithstanding the effects I allude to above) this is a set voltage (or more acurately change in voltage) - and I can't immediately think of any adaptation mechanisms that change this threshold. More likely you change RMP and therefore change the required size of a graded potential required to reach threshold.

    Now for your first statement - "So from what I understand i, when there is chronic depolarization, the absolute refractory period is not occuring and there is always depolarization, "

    No - with chronic depolarization of sufficient magnitude - there is a permanent refreactory period - hence why we cannot get another AP. Incidentally there are a bunch more subtleties we have to talk about, e.g. we are talking about a population of channels with very similar but not identicle biophysical properties, so e.g. even at RMP in the squid axon something like 30% of sodium channels have their h gates closed and cannot respond during an AP, so the resulting AP is not as big as it could be!! More to think about!
  9. Feb 17, 2011 #8
    I had also said in my first erased message - please do not think that the discussion above relates to a major mechanism of sensory nerve adaptation. I have little clue about sensory apparatus and how they desensitize (that will differ greatly from different sensory mechanisms) - I was merely coming to this discussion with info on how nerve accomodation has been experimentally shown - and can be seen clinically in some cases.
  10. Feb 19, 2011 #9
    Thanks again mtc1973. However can you elaborate on this "No - with chronic depolarization of sufficient magnitude - there is a permanent refreactory period". I tried to work it out but I don't get it.
  11. Feb 19, 2011 #10
    Lets say that our threshold potential is -70 mV and that our RMP is -80 mV. To trigger an AP we therefore need a 10 mV depolarization then we get the opening of Na channels (their m gates open). As sodium flows in and the cell depolarises the h gates will then be triggered to close, and sodium influx will stop. At the same time that this is happening the K channels are slowly building their conductance, their conductance becomes dominant as the Na channels close - hyperpolarizing the membrane potential to say e.g -85 mV.
    Now imagine that the h gate of the sodium channel needs the membrane potential to reach -85 mV before it resets. Essentially, then the hyperpolarization to -85 mV is necessary to reset the Na channel to be able to sustain the next action potential.
    But lets imagine that the external K is higher than normal - thus depolarizing the RMP to e.g. -72 mV. We now only need a 2 mV depolarization to trigger an action potential - but in the hyperpolarizing phase - the potential will never get to -85mV because of the raised extracellular K. Therefore the sodium channel h gates will remain closed and never reset - so no further action potentias are possible - i.e. a permanent extension of the refractory period.

    Very easy with a diagram - but I dont have time to draw one!! See if that makes sense - if not I'll find time to draw out a quick graph.
  12. Feb 20, 2011 #11
    Thanks mtc1973 :smile: I sort of understand. But why does extracellular K+ increase in chronic depolarization, I can understand they constantly move out of cell, but wouldn't the sodium potassium pump bring back K+ and restore the gradient. Also how does heart maintain,constant depolarization, if this mechanism occurs. Thanks!!
  13. Feb 21, 2011 #12
    OKay - think the other way round. Hyperkalemia causes depolarization, why do we get hyperkalemia - many different reasons! Can be related to kidney function, exercise, insulin problems - many reasons.
    MOst cells when bathed in extracellular fluid that has higher than normal K will become depolarized (since most cells have a high permeability to K).So it is not a situation that needs to be maintained - it just is, on account of the reduced K gradient across the cell membrane.
    So too little K leads to less excitability in heart and muscle since RMP is so far away from threshold. And too much K leads to reduced excitability in heart and muscle due to depolarized RMP and a larger population of Na channels having their h gates closed!
  14. Feb 21, 2011 #13
    Thanks again :smile: . After reading your previous replies I now understand how hyperkalaemia can reduce excitability, but it can also increase excitability because RMP is closer to threshold. So if there is question saying hyperkalaemia reduces excitability, is it true or false.

    Also from the quoted explanation. How does chronic depolarization cause a permanent refractory period. I understand how hyperkalaemia would stop the resetting of gates, but what do you mean when you say let's imagine K+ is higher than normal. In chronic depolarization why does hyperkalaemia occur. I'm talking about like a sensory stimulus applied for some time, how does it cause hyperkalaemia.
  15. Feb 21, 2011 #14
    Well, it can do either! Generally chronic depolarization due to hyperkalemia results in muscle weakness and paralysis, due to the inhibitory effects on the voltage gates Na channel. But initially you may well see increased excitability. So no clear answer - what you see clinically is what you see - but either is explicable.

    Because one gate of the Na channel is now closed (h gate) - it means that we cannot sustain an action potential even if threshold is reached. What is refractory period? - the time that a neuron is unable to sustain another action potential due to the inherent gate cycling of the Na channel. If that gate cycling is locked - then the Na channel is locked in its refractory state. Hence no further AP's. (Incidentally - this is exactly how neuromuscular blockers like succinylcholine work).

    it doesn't - I was stating that in hyperkalemia - chronic depolarization occurs. Not the other way round. I was thinking of a clinical reason for chronic depolarization - and hyperkalemia is one such clinical scenario. Depolarization is not the cause of hyperkalemia - but hyperkalemia is a cause of depolarization!

    And no - hyperkalemia would not occur due to prolonged sensory stimulus!
  16. Feb 25, 2011 #15
    Oh I see. Thanks for the help, I didn't know these things before, now I finally understand how absolute refractory period occur and why it is absolute :smile:
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