 Hello and welcome to Physiology Open. Nerve impulse is generated at Exxon-Hilox and then conducted along the length of Exxon to its terminal end. Conduction of nerve impulse is basically conduction of voltage change. This occurs by flow of charges from one point to other. But whenever charges flow, there is always drop in potential due to the resistance which the charges face while traveling. It's like at the electricity generation source, the power is in kV. But by the time it reaches the houses, it is much less. So there is a drop of potential while it travels through wires. So if action potential travels by this method, its amplitude will decrease over distance and finally there will be loss of all potential. That means action potential will not reach to the Exxon terminal. But does that happen? No. But if it is a graded change in potential, it does die down. That is, its amplitude decreases as it travels along the tendride. How is this happening? You will be surprised to know that action potential amplitude would decrease if it's only passive travel along that zone. Instead, a new action potential is being regenerated throughout the length of Exxon due to biological phenomena. So there are two things involved. One, passive travel of charges which changes the voltage in nearby regions. This depends on passive properties of membrane, that is input resistance, capacitance and exoplasmic resistance. And secondly, if the potential change reaches a threshold, there is regeneration of action potential at the new site. This depends on active properties of the membrane, that is opening of voltage catered sodium channel. And this process of passive change and then active generation of action potential repeats over the length of the Exxon. So now let's see how passive properties of a neuron affect the nerve impulse conduction. Fundamentally, for effective transmission, we want two things to happen. One, flow of charges with loss of least potential, so that the potential reaches the threshold in the neighboring region. Then this flow of charges should quickly change the potential of the nearby areas so that it reaches threshold quickly. So one is about the magnitude of potential and the second is about the speed of this magnitude change. So to understand this, let's divide the Exxon into sections. We will take both unmyelinated and myelinated neuron. Unmyelinated neuron, we will divide into smaller section while since myelinated neuron is covered with myelin sheet, which is interrupted every 1 to 2 millimeter, we will divide it into likewise segments. Before we proceed, one formula if you remember from physics, that a voltage change is directly dependent on the amount of charge at the site and inversely to the capacitance of that site. So clearly more charge at the site means more voltage change. Now flow of charges from one region to another depends on axoplasmic resistance, which is the resistance offered by the cytoplasm to the flow of charges. See as charges move along the length of the exon, they actually collide with each other. This leads to resistance and hence loss of potential. This resistance varies depending on the diameter of the axon. More the diameter, lesser the resistance and hence lesser loss of potential. So say for thinner neuron, it will cause lesser charge change in the neighboring region compared to a thicker neuron in the same time. But apart from this, there is one more factor which affects how much charge is there at the new site. It is input resistance of the membrane. See membrane has leaky channels and some amount of charge which reaches to the next region leaks out, preventing the buildup of the potential. If more charge leaks out, the membrane is said to have lower input resistance. Lesser leaking means high input resistance. So if leak is less, that is high input resistance, more charge will be there at the new site causing more change in potential magnitude. Hence amount of charge at a site depends on axoplasmic resistance and input resistance of the membrane. Now with the amplitude of action potential which is at this original site, even with the loss of charges, the potential change which occurs in nearby region reaches the threshold and leads to generation of new action potential. So in unmyelinated neuron, generation of action potential occurs at very close distances. For this to occur, there is very high density of voltage gated sodium channels throughout the length of the axon. However, this doesn't happen in a myelinated neuron. A myelinated axon is covered with myelin which is interrupted every 1 to 2 millimeters length. And these interruptions are known as nodes of randere which have high density of voltage gated channels. So in myelinated neuron, action potential regenerates only at nodes of randere. So potential loss will occur in the myelinated region, isn't it? Then is this good or bad? Well, because of myelination, potential loss is not much. This happens because myelination actually insulates the neuron. That is, there are no leaky channels here. So basically, loss of potential is less. Hence, the decay of potential to below threshold happens over a longer length as compared to what will happen in an unmyelinated neuron. But still, even with myelination, it cannot travel the entire length of axon without getting regenerated. Hence, the myelinated is interrupted in between and action potential regenerates every 1 to 2 millimeters. On the other hand, in non-myelinated neurons, since there is no insulation, potential loss will be too much by electronic conduction. And hence, at very close distances, action potential needs to be regenerated. That's why a non-myelinated nerve has high density of voltage gated channels across its entire length. Myelination does one more thing also. Apart from making sure that there is lesser potential loss, it also increases the speed of conduction. See, for potential change to occur, the charge should deposit on the membrane. This is similar as a capacitor. When the charge charges the capacitor, the potential change occurs. So it takes some time to charge the capacitor. Thicker the capacitor plates, less is the capacitance and it takes lesser time to change the potential. So, since myelination makes the membrane thicker, it actually decreases the capacitance. Thus, potential changes are faster. In fact, it is so fast that it appears that potential change just sweeps at the site of myelination. So, let's come back at the beginning two things. So, we wanted adequate magnitude of change in potential which should occur quickly. Now, increase in diameter of the neuron and myelination are two strategies by which conduction speed is increased. Due to increased diameter, anzoplasmic resistance decreases, causing effective flow of charges and loss of charges is prevented by myelination which basically insulates the membrane and decreases the leaky channels. While quick change of potential is again done by two things. One by decreasing axoplasmic resistance by increasing the diameter, this causes more charge to flow, causing faster change in potential to the threshold in the nearby areas. And secondly, by decreasing the capacitance by myelination. In summary, in non-myelinated neuron, the action potential spreads by electronic conduction which in turn leads to action potential regeneration at very closely spaced points. Otherwise, the potential loss will be too much over the length of exon and hence this strategy of action potential regeneration works in non-myelinated neuron. On the other hand in myelinated neuron, potential loss is lesser in the myelinated region and hence action potential is regenerated only at the nodes of ran wear. Also, the electronic conduction is much faster in the myelinated region. So, the potential just sweeps through the myelinated region and slows down only at nodes of ran wear where action potential is being regenerated. Due to this very fast conduction at myelinated regions, it appears action potential is jumping from node to node. This is known as saltatory conduction. Okay. Thanks for watching the video. If you liked it, do subscribe to the channel Physiology Open. Thank you.