Motor nerves

Local anesthetics produce anesthesia by blocking nerve impulse conduction in sensory, as well as motor nerve, fibers. Nerve impulses are initiated by membrane depolarization, effected by the opening of a sodium ion channel and an influx of sodium ions. Local anesthetics act by inhibiting the channel s opening they bind to a receptor located in the channel s interior. The degree of blockage on an isolated nerve depends not only on the amount of dmg, but also on the rate of nerve stimulation (153—156). 

PuAEMACoLOGiCAL AcTiox. Curare is stated to be almost inert when taken by mouth, owing to poor absorption by intestinal mucous membrane and the rapidity of elimination. Injected hypodermically it is a rapid and potent poison, paralysing the motor nerve-endings in striped muscle, so that voluntary movements cease and death occurs from respiratory failure. 

Cholinergic neurotransmission ChEs terminate cholinergic transmission in the central nervous system (CNS), in NMJs and in the autonomic system (the parasympathetic system, somatic motor nerves and pre-ganglionic sympathetic nerves). A few sensory cells and the NMJ in nematodes also include ChEs. 

Isaacs syndrome (an acquired neuromyotonia) is caused by autoantibodies directed against 4-aminopyr-idine or a-dendrotoxin-sensitive K+ channels (Kvl.l and Kvl.6) in motor and sensory neurons. The syndromes include muscle twitching during rest, cramps during muscle contraction, impaired muscle relaxation, and muscle weakness due to hyperexcitability of peripheral motor nerves. 

ATP with calcitonin gene-related peptide and substance P in sensory-motor nerves... 

The act of vomiting is a complex process accompanied by several events apart from activation of the motor nerves and various voluntary muscles involved in the increase of intragastric pressure and evacuation of the stomach contents. Vomiting is preceded by a deep inspiration, closure of the glottis and raising of the soft palate to prevent vomitus entering the trachea and nasopharynx, respectively. There is also increased heart rate, pallor, salivation, sweating and lacrimation. 

Muscle contraction is initiated by a signal from a motor nerve. This triggers an action potential, which is propagated along the muscle plasma membrane to the T-tubule system and the sarcotubular reticulum, where a sudden large electrically excited release of Ca " into the cytosol occurs. Accessory proteins closely associated with actin (troponins T, I, and C) together with tropomyosin mediate the Ca -dependent motor command within the sarcomere. Other accessory proteins (titin, nebulin, myomesin, etc.) serve to provide the myofibril with both stability... 

The smooth muscle cell does not respond in an all-or-none manner, but instead its contractile state is a variable compromise between diverse regulatory influences. While a vertebrate skeletal muscle fiber is at complete rest unless activated by a motor nerve, regulation of the contractile activity of a smooth muscle cell is more complex. First, the smooth muscle cell typically receives input from many different kinds of nerve fibers. The various cell membrane receptors in turn activate different intracellular signal-transduction pathways which may affect (a) membrane channels, and hence, electrical activity (b) calcium storage or release or (c) the proteins of the contractile machinery. While each have their own biochemically specific ways, the actual mechanisms are for the most part known only in outline. 

Voluntary muscle contraction is initiated in the brain-eliciting action potentials which are transmitted via motor nerves to the neuromuscular junction where acetylcholine is released causing a depolarization of the muscle cell membrane. An action potential is formed which is spread over the surface membrane and into the transverse (T) tubular system. The action potential in the T-tubular system triggers Ca " release from the sarcoplasmic reticulum (SR) into the myoplasm where Ca " binds to troponin C and activates actin. This results in crossbridge formation between actin and myosin and muscle contraction. 

Tetanus occurs when Cl. tetani, ubiquitous in the soil and faeces, contaminates wounds, especially deep puncture-type lesions. These might be minor traumas such as a splinter, or major ones such as battle injury. At these sites, tissue necrosis and possibly microbial growth reduce the oxygen tension to allow this anaerobe to multiply. Its growth is accompanied by the production of a highly potent toxin which passes up peripheral nerves and diSuses locally within the central nervous system. It acts like strychnine by affecting normal function at the synapses. Since the motor nerves of the brain stem are the shortest, the cranial nerves are the first affected, with twitches of the eyes and spasms of the jaw (lockjaw). 

Searle, T, Prior, C and Marshall, IG (1991) Acetylcholine recycling and release at rat motor nerve terminals studied using (— )-vesamicol and troxpyrrolium. J. Physiol. 444 99-116. 

Since ACh is the transmitter at the skeletal neuromuscular junction one might also expect it to be released from any axon collaterals arising from the motor nerve to it. Such collaterals innervate (drive) an interneuron (the Renshaw cell) in the ventral horn of the spinal cord, which provides an inhibitory feedback onto the motoneuron. Not... 

Muijser H, Hoogendijk EM, Hooisma J, et al. 1987. Lead exposure during demolition of a steel structure coated with lead-based paints. II. Reversible changes in the conduction velocity of the motor nerves in transiently exposed workers. Scand J Work Environ Health 13 56-61. 

The first identified Ascaris FaRP, AF1 (KNEFIRFamide), and the structurally related peptide, AF2 (KHEYLRFamide), have been found to inhibit locomotory waves when injected into adult worms (Cowden et al., 1989 Cowden and Stretton, 1993). Their effects on body-wall muscle strips are biphasic, comprising a transient relaxation followed by an extended period of increased contractile activity (Maule et al., 1995b Bowman et al., 1996). When using muscle strips that have had the motor nerve cords removed, only the inhibitory actions of AF1 and AF2 are seen (Maule et al., 1995b). This suggests that the inhibitory phase is due to post-synaptic effects on body-wall muscle in the worm. In contrast, the excitatory effects are nerve-cord dependent and are not observed in muscle strips that have been denervated. Another possibility is that the peptides interact with receptors at the post-synaptic junction - these are also removed in specimens that have had the motor nerve cords removed. 

Fig. 9.2 A general impression of the construction of nerve cells (a) cross-section of a nerve trunk, (b) a neuron, (c) sensory and motor nerve connection via a synapse.

Quantal analysis defines the mechanism of release as exocytosis. Stimulation of the motor neuron causes a large depolarization of the motor end plate. In 1952, Fatt and Katz [11] observed that spontaneous potentials of approximately 1 mV occur at the motor endplate. Each individual potential change has a time course similar to the much larger evoked response of the muscle membrane that results from electrical stimulation of the motor nerve. These small spontaneous potentials were therefore called... 

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