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somasimple
Gold Member
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Hi All,
I took the following from this page. http://en.wikipedia.org/wiki/Action_potential
I'm lost with these comments because I learned that small fibres have low speed and larger ones have a higher one but, in my opinion, since membrane thickness doesn't really vary in unmyelinated axons, capacity is enlarged!
That seems to contradict the wiki?
I took the following from this page. http://en.wikipedia.org/wiki/Action_potential
The action potential
When a stimulus arrives at a receptor or nerve ending, its energy causes a temporary reversal of the charges on the neuron cell surface membrane. As a result, the negative charge of 70 mV inside the membrane becomes a positive charge of around +40mV. This is known as the action potential, and in this condition the membrane is said to be depolarised. (See depolarization) This depolarization occurs because channels in the axon membrane change shape, and hence open or close, depending on the voltage across the membrane. They are therefore called voltage-gated ion channels. The sequence of events is described below.
1. At resting potential some potassium leak channels are open but the voltage-gated sodium channels are closed. Potassium diffusing down the potassium concentration gradient creates a negative-inside membrane potential.
2. A local membrane depolarization caused by an excitatory stimulus causes some voltage-gated sodium channels in the neuron cell surface membrane to open and therefore sodium ions diffuse in through the channels along their electrochemical gradient. Being positively charged, they begin a reversal in the potential difference across the membrane from negaitve-inside to positive-inside. Initially, the inward movement of sodium ions is also favored by the negative-inside membrane potential.
3. As sodium ions enter and the membrane potential becomes less negative, more sodium channels open, causing an even greater influx of sodium ions. This is an example of positive feedback. As more sodium channels open, the sodium current dominates over the potassium leak current and the membrane potential becomes positive inside.
4. Once a membrane potential of around +40 mV has been established, voltage-sensitive inactivation gates of the sodium channels, sensitive to the now positive membrane potential gradient, close (so further influx of sodium is prevented). While this occurs, the voltage-sensitive activation gates on the voltage-gated potassium channels begin to open.
5. As voltage-gated potassium channels open and there is a large outward movement of potassium ions driven by the potassium concentration gradient and initially favored by the positive-inside electrical gradient. As potassium ions diffuse out, this movement of positive charge causes a reversal of the membrane potential to negative-inside and repolarisation of the neuron back towards the large negative-inside resting potential.
6. The large outward current of potassium ions through the voltage-gated potssium channels causes the temporary overshoot of the electrical gradient, with the inside of the neuron being even more negative (relative to the outside) than the usual resting potential. This is called hyperpolarisation (hyperpolarization). The voltage-sensitive inactivation gates on the potassium channels now close and the continual movement of potassium through potassium leak channels again dominates the membrane potential. Sodium-potassium pumps continue to pump sodium ions out and potassium ions in, preventing any long-term loss of the ion gradients. The resting potential of -70 mV is re-established and the neuron is said to be repolarised.
Propagation
Propagating action potentials can be modeled by joining several RC circuits, each one representing a patch of membrane.
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Propagating action potentials can be modeled by joining several RC circuits, each one representing a patch of membrane.
In unmyelinated axons, action potentials propagate as an interaction between passively spreading membrane depolarization and voltage-gated sodium channels. When one patch of cell membrane is depolarized enough to open its voltage-gated sodium channels, sodium ions enter the cell by facilitated diffusion. Once inside, positively-charged sodium ions "nudge" adjacent ions down the axon by electrostatic repulsion (analogous to the principle behind Newton's cradle) and attract negative ions away from the adjacent membrane. As a result, a wave of positivity moves down the axon without any individual ion moving very far. Once the adjacent patch of membrane is depolarized, the voltage-gated sodium channels in that patch open, regenerating the cycle. The process repeats itself down the length of the axon, with an action potential regenerated at each segment of membrane.
The main impediment to conduction speed in unmyelinated axons is membrane capacitance. In an electric circuit, the capacity of a capacitor can be decreased by decreasing the cross-sectional area of its plates, or by increasing the distance between plates.
I'm lost with these comments because I learned that small fibres have low speed and larger ones have a higher one but, in my opinion, since membrane thickness doesn't really vary in unmyelinated axons, capacity is enlarged!
That seems to contradict the wiki?