Demonstrates the uniqueness of shrimp nerve fibers with fastest conduction velocity in the animal kingdom. Compares distant branches of the evolutionary tree with different morphogenesis but similar outcome. The peculiar myelin sheath with its unique nodal structure and the electrical properties of the nerve fibers of the shrimp have continued to be investigated for a quarter of century and are now fully described in this book.
In the shrimp, researchers found a completely novel type of functional node in the giant fiber which they designated as the fenestration node. In portions of the myelinated fiber, the fenestration node furnished the sites of excitation.
Also discovered was a new strategy for increasing impulse conduction in the shrimp. The book includes a section on the formation of the fenestration node and the discovery of a strategy that allows the shrimp to escape its predators by an action of the fastest velocity. When the cell is at rest, and the ion channels are closed except for leakage channels which randomly open , ions are distributed across the membrane in a very predictable way.
The cytosol contains a high concentration of anions, in the form of phosphate ions and negatively charged proteins. Large anions are a component of the inner cell membrane, including specialized phospholipids and proteins associated with the inner leaflet of the membrane leaflet is a term used for one side of the lipid bilayer membrane. The negative charge is localized in the large anions.
With the ions distributed across the membrane at these concentrations, the difference in charge is measured at mV, the value described as the resting membrane potential.
The exact value measured for the resting membrane potential varies between cells, but mV is most commonly used as this value. This voltage would actually be much lower except for the contributions of some important proteins in the membrane. This may appear to be a waste of energy, but each has a role in maintaining the membrane potential.
Resting membrane potential describes the steady state of the cell, which is a dynamic process that is balanced by ion leakage and ion pumping. Without any outside influence, it will not change. To get an electrical signal started, the membrane potential has to change. Because sodium is a positively charged ion, it will change the relative voltage immediately inside the cell relative to immediately outside.
The resting potential is the state of the membrane at a voltage of mV, so the sodium cation entering the cell will cause it to become less negative. This is known as depolarization , meaning the membrane potential moves toward zero.
The electrical gradient also plays a role, as negative proteins below the membrane attract the sodium ion. These channels are specific for the potassium ion. This is called repolarization , meaning that the membrane voltage moves back toward the mV value of the resting membrane potential. Repolarization returns the membrane potential to the mV value that indicates the resting potential, but it actually overshoots that value.
What has been described here is the action potential, which is presented as a graph of voltage over time in Figure 8. It is the electrical signal that nervous tissue generates for communication. That can also be written as a 0. To put that value in perspective, think about a battery. An AA battery that you might find in a television remote has a voltage of 1.
The change seen in the action potential is one or two orders of magnitude less than the charge in these batteries.
In fact, the membrane potential can be described as a battery. A charge is stored across the membrane that can be released under the correct conditions. What happens across the membrane of an electrically active cell is a dynamic process that is hard to visualize with static images or through text descriptions. View this animation to learn more about this process.
And what is similar about the movement of these two ions? The question is, now, what initiates the action potential? The description above conveniently glosses over that point.
But it is vital to understanding what is happening. The membrane potential will stay at the resting voltage until something changes. Instead, it means that one kind of channel opens. Whether it is a neurotransmitter binding to its receptor protein or a sensory stimulus activating a sensory receptor cell, some stimulus gets the process started. Sodium starts to enter the cell and the membrane becomes less negative. The channels that start depolarizing the membrane because of a stimulus help the cell to depolarize from mV to mV.
This is what is known as the threshold. Any depolarization that does not change the membrane potential to mV or higher will not reach threshold and thus will not result in an action potential. Also, any stimulus that depolarizes the membrane to mV or beyond will cause a large number of channels to open and an action potential will be initiated.
Because of the threshold, the action potential can be likened to a digital event—it either happens or it does not. If the threshold is not reached, then no action potential occurs. Also, those changes are the same for every action potential, which means that once the threshold is reached, the exact same thing happens. Stronger stimuli will initiate multiple action potentials more quickly, but the individual signals are not bigger.
Thus, for example, you will not feel a greater sensation of pain, or have a stronger muscle contraction, because of the size of the action potential because they are not different sizes. The action potential is initiated at the beginning of the axon, at what is called the initial segment. Because of this, depolarization spreading back toward previously opened channels has no effect.
The action potential must propagate toward the axon terminals; as a result, the polarity of the neuron is maintained, as mentioned above. Propagation, as described above, applies to unmyelinated axons. When myelination is present, the action potential propagates differently. Because there is not constant opening of these channels along the axon segment, the depolarization spreads at an optimal speed.
Drugs such as digitalis , which increase vagal activity to the heart, are sometimes used to reduce AV nodal conduction in patients that have atrial flutter or fibrillation. These atrial arrhythmias lead to excessive ventricular rate tachycardia that can be suppressed by partially blocking impulses being conducted through the AV node.
Phase 0 of action potentials at the AV node is not dependent on fast sodium channels as in non-nodal tissue , but instead is generated by the entry of calcium into the cell through slow-inward, L-type calcium channels. Blocking these channels with a calcium-channel blocker such as verapamil or diltiazem reduces the conduction velocity of impulses through the AV node and can produce AV block. Because conduction velocity depends on the rate of tissue depolarization, which is related to the slope of phase 0 of the action potential, conditions or drugs that alter phase 0 will affect conduction velocity.
For example, conduction can be altered by changes in membrane potential, which can occur during myocardial ischemia and hypoxia.
These membrane changes result in a decrease in speed by which action potentials are conducted within the heart. This can have a number of consequences. First, activation of the heart will be delayed, and in some cases, the sequence of activation will be altered. This can seriously impair ventricular pressure development. Second, damage to the conducting system can precipitate tachyarrhythmias by reentry mechanisms.
Click here to learn more about altered impulse conduction. Antiarrhythmic drugs such as quinidine a Class IA antiarrhythmic that block fast sodium channels cause a decrease in conduction velocity in non-nodal tissue. Cardiovascular Physiology Concepts Richard E.
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