# Excitation conduction

When conduction in the will of Animal Physiology and Medicine forwarding a excitation in nerve cells or muscle cells , the transmission of a designated, for example in neuron action potential along the neurites , which in different ways as axon of glial cells can be coated. Depending on the design of this glial envelope, different types of conduction are possible; The conduction speed of the nerve fiber is considerably increased by a strongly developed myelin sheath .

An excitation can be transmitted quickly over very short distances by electrotonics , but with a decreasing voltage difference . For greater distances, therefore, the repeated formation of action potentials by ion currents is necessary, which can happen continuously and progressively. Only sufficient isolation through multiple myelin-containing wraps allows a step-by-step process in which a depolarization electrotonically transmitted over short isolated sections ( internodes ) alternates with the build-up of action potentials on the axon membrane area that is exposed in between ( Ranvierscher Schnürring ).

The term "stimulus conduction", which is occasionally used, is incorrect because it is not the stimulus that is passed on, but an excitation caused by it.

## Basics

Fig. 1: Schematic representation of the resistances and capacities on an axon.

In simplified terms, an axon can be viewed as a long cylinder consisting of a series of sections. The wall of this cylinder is formed by the lipid bilayer of the axon membrane, whose electrical properties can be described as the parallel connection of a resistor and a capacitor with the capacitance . The electrical resistance of the membrane in the unexcited state is so great that the lipid bilayer fulfills the function of a dielectric , so that a capacitance is created by the electrostatic forces that are effective across the membrane between the intra- and extracellular space . Their size is proportional to the surface area of ​​the membrane and inversely proportional to its thickness. ${\ displaystyle r_ {m}}$ ${\ displaystyle c_ {m}}$${\ displaystyle c_ {m}}$

### Membrane time constant

If the axon is not excited, it has a resting membrane potential of approx. −70 mV, which means that this potential difference exists between the two plates of the capacitor . The membrane potential changes during a depolarization; the capacitor has to be discharged - or even recharged if the potential difference becomes positive. The time required for this process can be determined with the help of the membrane time constant and is calculated as the product of the membrane resistance and the membrane capacity : ${\ displaystyle \ tau}$${\ displaystyle r_ {m}}$${\ displaystyle c_ {m}}$

${\ displaystyle \ tau = r_ {m} \ cdot c_ {m}}$.

The time constant indicates the time in seconds for the exponential process, after which the amplitude of the potential difference has dropped to 1 / e or about 36.8% of the initial value or reduced by the factor ; this constant is therefore a measure of the speed of the change in potential. Since this process of actually time-consuming for the propagation of excitation is - and, for each membrane section which is depolarized, repeated needs - the conduction can be accelerated when the membrane time constant is reduced or decreases the frequency with which an action potential again must be formed. The latter is made possible by increasing the lengthwise constant membrane described below . ${\ displaystyle \ tau}$${\ displaystyle e}$

### Longitudinal membrane constant

Fig. 2: Change in the membrane potential for two axons with different membrane longitudinal constants after triggering an action potential with increasing distance from the location of excitation.

In addition to the longitudinal resistance, each axon also has a membrane resistance . Together with the longitudinal resistance , a membrane longitudinal constant is calculated from this . It indicates the distance along an axon after which the amplitude of the potential has dropped to 36.8%. From this it can be deduced that the distance after which an action potential triggered at a location is still able to trigger an action potential again by opening voltage-dependent cation channels, the greater the greater the membrane longitudinal constant. According to the above equation, it can be increased on the one hand by increasing the membrane resistance. In the human organism this happens through the isolation of the axon through myelination, which reduces the occurrence of leakage currents and thus minimizes the loss of the charge carriers that are responsible for the formation of the potential difference. On the other hand, the membrane longitudinal constant can be increased by reducing the longitudinal resistance. It is inversely proportional to the cross-sectional area of ​​the axon: a doubling of the axon diameter leads to a decrease in the longitudinal resistance to a quarter. However, since the membrane capacity increases and the membrane resistance decreases due to the increasing surface area of ​​the axon, the effect on the conduction velocity is less in practice. ${\ displaystyle r_ {m}}$${\ displaystyle r_ {l}}$${\ displaystyle \ lambda}$

## Electrotonic excitation conduction

Fig. 3: Electrotonic excitation line

The electrotonic transmission carries an excitation on quickly, but only over very short distances. Since the membrane around the axon is a relatively poor insulator, the electrical potential decreases with increasing distance. An example of electrotonic excitation can be found in the human retina . Here the excitation is passed on electrotonically as a graduated, stimulus-analogous potential change. This applies to both the photoreceptors and the bipolar cells ; Action potentials are only formed in the ganglion cells . The electrotonic form of the excitation conduction seldom extends beyond a few hundredths of a millimeter due to the unfavorable conditions of the ion conduction inside the axon with little insulation to the outside. If the potential is then raised again by action potentials, further transmission of the signals is possible.

## Stimulus conduction through action potentials

In axons of nerve cells , sufficient depolarization causes the temporary opening of voltage-activated sodium channels in the membrane . A depolarization wave running over the axolemm can thus lead to action potentials, which are passed on via the nerve fiber . Depending on whether the axon is myelinated or not, two ways can be distinguished:

### Continuous conduction of excitation

Fig. 4a: Continuous excitation conduction

In the case of nerve fibers without myelination, the so-called unmarked nerve fibers , impulses can be passed along the axon by continuously triggering action potentials starting from an excited axon area and across the neighboring areas. While the newly excited membrane section was electrotonically depolarized and above the threshold potential, changing its permeability , an action potential begins to develop, the excitation in the previous section already subsides and goes into the re -polarization phase . This form of transmission of excitations as an action potential that is continuously formed is relatively slow (usually only 1–3 m / s, maximum 30 m / s) and is found quite often in nerves that supply internal organs . Nociceptors with fiber diameters of less than one micrometer also show low line speeds . However, the conduction velocity can be increased by thickening the axon. In this context, the well-studied so-called giant axons in cuttlefish and marine snails of the genus Aplysia with diameters of up to one millimeter are particularly known . The larger diameter accelerates their signal transmission; not very effective, however, since the reduced longitudinal resistance is offset by an increased membrane capacity and a reduced membrane resistance (see above ).

### Saltatory excitation conduction

Fig. 4b: Saltatory excitation conduction
Fig. 5: Membrane potential (top) and time course (bottom) as a function of the distance covered along an axon (middle) in the saltatory conduction.

In vertebrates, most of the axons are covered by a myelin sheath ( medullary nerve fiber ), which is formed by Schwann cells in the peripheral nervous system or by oligodendrocytes in the central nervous system and which is interrupted at intervals of 0.2 mm to 1.5 mm. Such an interruption is called a nodus, knot or Ranvierscher Schnürring . The myelinated, i.e. H. isolated section, is called internode . This isolation increases the longitudinal membrane constant (see above) of the axon from a few hundredths of a millimeter to a few millimeters. Since the insulation also leads to a reduction in the electrical capacitance from around 300 nF / m to around 0.8 nF / m, the membrane time constant is also reduced. This effect alone enables real transmission speeds of over 100 m / s with an unchanged cross-section of the axon. In addition, there are voltage-dependent Na + channels and Na + / K + -ATPases in a 100-fold higher density on the cord rings. All these components make it possible that an action potential, which was generated on a cord up to 1.5 mm away, depolarizes the membrane on the next cord enough to trigger another action potential there. The exact electrophysiological processes that take place are described below by way of example.

On the unexcited nerve fiber, the resting membrane potential prevails at every point along the axon, which in Figure 5 is −90 mV. This means that there is a potential difference between the intra- and extracellular space; along the axon, e.g. B. between N 1 and N 2 , this is not the case. If an excitation in the form of an action potential arrives at the first ring N 1 , which depolarizes the membrane above the threshold potential, which is −60 mV in Figure 5, voltage-dependent Na + channels open. Following their electrochemical gradient , Na + ions now flow from the extra- into the intracellular space of the axon. This leads to the depolarization of the plasma membrane in the area of ​​the constriction ring N 1 , i.e. the capacitor formed by the membrane (see basics) is recharged to +30 mV in Figure 5. A time of about 0.1 ms is required for this process, which depends on the membrane time constant already explained in the section on the fundamentals. The influx of positively charged sodium ions resulted in an intracellular excess of positive charge carriers at N 1 compared to the surroundings. This immediately results in the formation of an electrical field and thus a potential difference along the axon: the resulting electrical field directly exerts a force on charged particles further away: negatively charged particles (e.g. Cl - ions experience at N 2) ) an attractive force in the direction of the positive excess charge at N 1 . At the same time, positive charge carriers located between N 1 and N 2 are moved in the direction of N 2 by the electric field . As a result of these charge shifts, there is almost no delay in a positiveization of the membrane potential at N 2 , namely without ions having to travel all the way from N 1 to N 2 . This process is comparable to switching on an incandescent lamp by pressing a remote light switch: The incandescent lamp begins to shine without delay because the electrons in the metal conductor are immediately set in motion everywhere and therefore a current is already flowing in the incandescent lamp, although every single one of them is flowing Electron has only moved a few hundredths of a millimeter.

As shown in Figure 5 below, the electrotonic propagation of the depolarization via the internode thus takes place almost without loss of time, while a relatively large amount of time has to be spent for the regeneration of the action potential on the cord rings. Since the excitation seems to jump from ring to ring, one speaks of a saltatory excitation conduction.

The membrane potential along the axon now runs as shown by the blue curve in Figure 5 and, with increasing distance from N 1, would approach the resting membrane potential more and more (dashed curve) if it were not due to the supra-threshold depolarization of the membrane at N 2 to open of the voltage-dependent Na + channels there. This leads to a regeneration of the action potential and a course of the membrane potential according to the purple curve until the processes described are repeated again at N 3 .

At a line speed of 120 m / s, a nerve impulse of 1 ms duration has a length of 120 mm. That means that when a pulse passes through, around 80 to several hundred cord rings are excited at the same time. At the front of the propagating electrical impulse there is a constant change between the electrotonic conduction in the internodes and the regeneration of the amplitude of the action potential in the cord rings.

At birth, the medullary sheaths are missing in some places in humans. So are z. B. the pyramidal tracts are not yet completely myelinated, which means that reflexes can be triggered in small children that are considered pathological (diseased) in adults (see Babinski reflex ). However, after two years, no more pathological reflexes should be observed. In the case of demyelinating diseases such as multiple sclerosis , the myelin sheaths are broken down in the central nervous system, which leads to a wide range of failure symptoms.

## Excitation transmission

If an action potential or a graduated depolarization reaches the presynaptic termination of an axon, this triggers a process sequence that leads to the fact that small vesicles ( synaptic vesicles ) fuse with the presynaptic membrane and the contained quantity of neurotransmitters are released into the synaptic gap ( exocytosis ). These transmitters can bind to specific receptors in the membrane of a postsynaptically assigned cell. Via this, ion channels in the postsynaptic membrane are opened for a short time either directly ligand-controlled ( ionotropic ) or indirectly mediated ( metabotropic ). The ion specificity of these channels decides whether the postsynaptic cell (nerve, muscle or glandular cell) is depolarized (excited) or hyperpolarized (inhibited). Depending on the type of cell response evoked by the transmitter via the receptor binding, either an exciting postsynaptic potential occurs locally in the subsequent cell, which is electrotonically passed on via the membrane, or an inhibitory one that hinders the transmission.

At the neuromuscular synapse of the skeletal muscle , the motor end plate as the connection point between a nerve cell and a muscle fiber , the transmitter acetylcholine is released from the vesicles and passes through the synaptic gap. The transmitter molecules are bound to receptor molecules on the membrane of the muscle cell ( sarcolemma ). Then (in this case) the acetylcholinesterase splits the acetylcholine transmitter into acetate and choline . The choline is taken up again through a choline channel in the presynaptic membrane, connected with acetic acid and stored again as acetylcholine in a vesicle.

## Spread of excitation in the heart

The spread of excitation in the heart is unique in the body due to the combination of the excitation conduction system and the transfer of excitation from cell to cell .

## literature

• Robert F. Schmidt, Hans-Georg Schaible: Neuro- and sensory physiology . 5th edition. Springer, Heidelberg 2006, ISBN 3-540-25700-4 .