Nerve impulse, propagation

Excitable media are some of tire most commonly observed reaction-diffusion systems in nature. An excitable system possesses a stable fixed point which responds to perturbations in a characteristic way small perturbations return quickly to tire fixed point, while larger perturbations tliat exceed a certain tlireshold value make a long excursion in concentration phase space before tire system returns to tire stable state. In many physical systems tliis behaviour is captured by tire dynamics of two concentration fields, a fast activator variable u witli cubic nullcline and a slow inhibitor variable u witli linear nullcline [31]. The FitzHugh-Nagumo equation [34], derived as a simple model for nerve impulse propagation but which can also apply to a chemical reaction scheme [35], is one of tire best known equations witli such activator-inlribitor kinetics ... 

FIGURE 30.4 Nerve impulse propagation by longitudinal currents in the extracellular solution and in the cytoplasm. 

A nerve impulse propagated along the axon must be transmitted across the synaptic cleft to be further propagated. An impulse does not come alone, but in a train of impulses. Because impulse transmission in an axon is an all-or-nothing phenomenon, it is the frequency and not the amplitude of each impulse that determines the strength of the signal. The mechanism, now fairly well understood, is described briefly. 

Local anesthetics are able to depress or block nerve conduction at low dosage Davis has demonstrated a relationship between antiarrhythmic potency, local anesthesia and neuromuscular transmission . The actions of antiarrhythmic agents to slow conduction can be explained by their depression of neuromuscular transmission. Slowed conduction can be explained through a retardation of the nerve impulse propagation, by increasing the electrical excitation threshold and reducing the rate of rise of the action potential . ... 

Choline functions in fat metaboHsm and transmethylation reactions. Acetylcholine functions as a neurotransmitter in certain portions of the nervous system. Acetylcholine is released by a stimulated nerve cell into the synapse and binds to the receptor site on the next nerve cell, causing propagation of the nerve impulse. 

Local anaesthetics are drugs that reversibly interrupt impulse propagation in peripheral nerves thus leading to autonomic nervous system blockade, analgesia, anaesthesia and motor blockade in a desired area of the organism. 

When large areas of the membrane are depolarized in this manner, the electrochemical disturbance propagates in wave-like form down the membrane, generating a nerve impulse. Myelin sheets, formed by Schwann cells, wrap around nerve fibers and provide an electrical insulator that surrounds most of the nerve and greatly speeds up the propagation of the wave (signal) by allowing ions to flow in and out of the membrane... 

A disadvantage of using synaptosomes is that they cannot be used to study transmitter release evoked by propagated nerve impulses, but the release, like that from intact neurons, is Ca +-dependent and K+-sensitive. Pharmacological studies using synaptosomes have also provided evidence that the amount of transmitter that is released following their depolarisation is regulated by the activation of presynaptic receptors. 

The idea that signals are transmitted along the nerve channels as an electric current had arisen as early as the middle of the nineteenth century. Yet even the first measurements performed by H. Helmholtz showed that the transmission speed is about lOm/s (i.e., much slower than electric current flow in conductors). It is known today that the propagation of nerve impulses along the axons of nerve cells (which in humans are as long as 1.5m) is associated with an excitation of the axon s outer membrane. 

Neuromuscular transmission (B) of motor nerve impulses to the striated muscle fiber takes place at the motor endplate. The nerve impulse liberates acetylcholine (ACh) from the axon terminal. ACh binds to nicotinic cholinocep-tors at the motor endplate. Activation of these receptors causes depolarization of the endplate, from which a propagated action potential (AP) is elicited in the surrounding sarcolemma. The AP triggers a release of Ca from its storage organelles, the sarcoplasmic reticulum (SR), within the muscle fiber the rise in Ca concentration induces a contraction of the myofilaments (electromechanical coupling). Meanwhile, ACh is hydrolyzed by acetylcholinesterase (p. 100) excitation of the endplate subsides. if no AP follows, Ca + is taken up again by the SR and the myofilaments relax. 

Alkali and alkaline-earth cations (AC and AEC) occupy an important position in matter and in life. In biology, they are present as charge carriers in ionic processes (cf. the role of Na+ and K+ in the propagation of the nerve impulse) and as structure holders (Mg2+, Ca2+). 

Recent drug development studies have centered on the capacity of known antiepileptic drugs (AEDs) to interact with ion channels, and it is now established that several agents appear to be exerting their effects primarily by inhibiting ion channels. Modulation of neuronal sodium channels decreases cellular excitability and the propagation of nerve impulses. Inhibition of sodium channels appears to be a major component of the mechanism of action of several anticonvulsant drugs. 

Local anesthetics preferentially block small fibers because the distance over which such fibers can passively propagate an electrical impulse is shorter. During the onset of local anesthesia, when short sections of a nerve are blocked, the small-diameter fibers are the first to fail to conduct electrical impulses. For myelinated nerves, at least two and preferably three successive nodes of Ranvier must be blocked by the local anesthetic to halt impulse propagation. Therefore, myelinated nerves tend to become blocked before unmyelinated nerves of the same diameter. For this reason, the preganglionic fibers are blocked before the smaller unmyelinated C fibers involved in pain transmission. 

Voltage-regulated sodium channels are the major participants in propagation of nerve impulses. Tire large 260-kDa a subunit of the sodium channel of nerve membranes contains four homologous repeat sequences, each of which may form transmembrane helices and also contain a loop that may participate in forming a pore similar to the K+ pore of Fig. 8-21.509 510a However, the structure is uncertain.511 Tire channel complex also contains 36- or 33-kDa Pj and P2 subunits that appear to be members of the Ig superfamily. 

Transducin, cyclic GMP, and phosphodiesterase. Tire essential consequence of light absorption is an alteration in the membrane potential in the vicinity of the absorbed photon with the resulting propagation of a nerve impulse down the plasma membrane to the synapse by cable conduction (Chapter 30). Tire type of potential change that is transmitted differs among vertebrates and invertebrates.522 In the case of mammalian photoreceptors the rod outer segment is permeable to sodium ions so that a large... 

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