Propagation of the Action Potential
Propagation of the Action Potential BIOH 313-001
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This 6 page Class Notes was uploaded by Rebeka Jones on Thursday September 29, 2016. The Class Notes belongs to BIOH 313-001 at Montana State University taught by Noudoost, Behrad in Fall 2016. Since its upload, it has received 4 views. For similar materials see Neurophysiology in Cell Biology and Neuroscience at Montana State University.
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Date Created: 09/29/16
Propagation of the action potential September, 29 2016 If the injected current does not depolarize the membrane to threshold, no action potentials will be generated. If injected current depolarizes the membrane beyond threshold, action potentials will be generated. The action potential firing rate increase as the depolarizing current increases Vm *what happens in the cell during each process of the action potential during the relative refractory period if you hit it with more depolarization you can open the sodium channel again….. *it should say closed on the chart during relative refractory period on voltage gated Na channel If you hit the inactivation gate with depolarization it will only close….so during the absolute refractory period (where it is already closed) you would just be making it close again in a sense…. that is why you can only reopen the gate during the relative refractory period. Threshold – membrane potential where enough voltage-gated sodium channels open so that the relative ionic permeability of the membrane favors sodium over potassium Rising phase – the inside of the membrane has negative electrical potential, there is a large drive force of Na+ ions. Therefore, Na+ ions rush into the cell through the open sodium channels, causing rapid depolarization of the membrane. Overshoot- relative permeability of the membrane greatly favors sodium; the membrane potential goes to a value close to E whina is greater than o mV. Falling phase – the behavior of two types of channel contribute to the falling phase First – voltage gate sodium channels inactivate Second – the voltage gated potassium channels finally open. There is a great driving force on K+ ions when the membrane is strongly depolariz ed. Therefore, K+ ions rush out of the cell through the open channels, causing the membrane potential to become negative again. Undershoot - the open potassium channels add to the resting potassium membrane permeability. Because there is very little sodium permeability, 2 the membrane potential goes toward E , causikg hyperpolarization relative to the resting membrane potential until the potassium channels close again. Absolute refractory period – sodium channels inactivate when the membrane becomes strongly depolarized. They cannot be activated again until the membrane potential goes sufficiently negative to de-inactivate the channels. Relative refractory period – The membrane potential stays hyperpolarized until the voltage gated potassium channels close. Therefore, more depolarizing current is required to bring the membrane to threshold. Action potential conduction require both active and passive current flow Passive propagation – When thinking about how an action potential travels down a neuron's axon, it is useful to think about an analogy of a television's volume. As you walk further and further away The sound coming from the speaker gets quieter and quieter. The strength of the decay is determined by time constant – the amount of time to reach desired voltage 3 it is related to the resistance of neuron membrane and capacitance of the membrane the higher the time constant the less desired neuron you have length constant – measure of how far the voltage travels down the axon before it decays to 0 (how much leaks out, more leakages more decay) it is related to neuron membrane resistance, depends on leakage channels and “cell size”. The higher the rm the signal leaks less as it travels *when there is myelin it changes membrane resistance by “blocking” the leaks and inversely related to axial resistance, depends on the size of the cell, (when this is bigger it will decay faster) the smaller the cross section of the axon the greater its axial resistance – therefore a larger axon has a smaller ra and therefore a larger length constant and thus signal travel with smaller decay and ideal neuron would have a high length constant and low time constant The presence of myelin increases rm Active propagation -activation of more voltage-gated channels down the road orthodromic = normal = from cell body to axon terminal antifromic = abnormal = from cell body to soma 4 in an artificial stimulation the signal will travel in both directions because there are no refractory periods behind the signal the signal is gradually decaying…..if it reaches another sodium voltage gated channel it can regenerate the action potential * The discrete regeneration of action potentials between lengths of myelin at the Nodes of Ranvier is called "saltatory conduction.” (from the Latin saltare, to jump) *movie found on D2L under experiment *important to know the ranges 5 Myelin is great but it is expensive *copied from presentation + + • Less energy must be expended by the Na -K pump in restoring the Na and K concentration gradients, which tend to run down as a result of action-potential activity. • The benefits of myelin substantially outweigh the benefits of axon diameter size. Tripling the myelin thickness increases the conduction velocity 3x, whereas tripling the axon diameter only increases the conduction velocity by the square root of 3, or 1.7 times. • There is a metabolic cost, however, to making myelin (you need to keep the special cells alive that coat the neurons in fat), so it's not the perfect solution for all animals. • Even the largest axons without myelin in the animal kingdom, such as the 1 mm diameter squid giant axon, only has a conduction velocity of 20-25 m/s second! You have myelinated axons in your body (the A alpha fibers) that are only 13-20 μm in diameter (1/100 of the size of the squid axon), yet have conduction velocities that are 80-120 m/s! Myelin is a wonderful biological invention, allowing neurons to get both small and fast, but it is expensive. • Various diseases of the nervous system, such as multiple sclerosis and Guillain-Barre syndrome, cause demyelination. Because the lack of myelin slows down the conduction of the action potential, these diseases can have devastating effects on behavior. As an action potential goes from a myelinated region to a bare stretch of axon the inward current generated at the node just before the demyelinated segment may be too small to provide the capacitive current required to depolarize the demyelinated membrane to threshold. In addition, this local-circuit current does not spread as far as it normally would because it is flowing into a segment of axon that, because of its low rm, has a short length constant. These two factors can combine to slow, and in some cases actually block, the conduction of action potentials. 6
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