Neuromuscular transmissions

Figure 1. A depiction of the several different ionic currents necessary for the acute function of neuromuscular transmission in the skeletal motor and the efferent autonomic nervous system. The boxed current designations are associated, by the arrows, with those cellular regions where their physiological role is most evident, although these currents often exist in other regions of the cell. = neurotransmitter-activated current ...

Martin, R.J., Pennington, A.J., Duittoz, A.H., Robertson, S. and Kusel, J.R. (1991) The physiology and pharmacology of neuromuscular-transmission in the nematode parasite, Ascaris suum. Parasitology 102, S41-S58. 

Katz, B. and Miledi, R. The timing of calcium action during neuromuscular transmission. J. Physiol. (Lond.) 189 535-544, 1967. 

Behavioral and motor effects Mescaline and its analogs inhibit cholinergic neuromuscular transmission by blocking release of acetylcholine and reducing end-plate potentials in the micromolar range (Ghansah et al. 1993). This effect has not been investigated in humans, but it could reduce the force of muscle contractions and motor control. 

Shoaib M. (1998). Is dopamine important in nicotine dependence J Physiol Paris. 92(3-4) 229-33. Sieb JP, Engel AG. (1993). Ephedrine effects on neuromuscular transmission. Brain Res. 623(1) 167-71. 

Ghansah E, Kopsombut P, Malleque MA, Brossi A. (1993). Effects of mescaline and some of its analogs on cholinergic neuromuscular transmission. Neuropharmacology. 32(2) 169-74. 

The MSAL-type alkaloids are potent neuromuscular poisons in mammals, acting at the post-synaptie neuromuseular junction. Variations in structural features of eaeh norditerpenoid alkaloid ean exaeerbate or reduee toxieity. While the mechanism of action of the norditerpenoid alkaloids involves blocking of neuromuscular transmission at the al nicotinic acetylcholine receptors, relative toxicity of individual alkaloids is observed to change with variations in the structural characteristics of the alkaloids (Dobelis et al., 1999). In comparison with the lyeoetonine and MDL-type alkaloids, the high toxicity... 

Pain, muscular weakness, cramps and ease of fatigue are the most usual symptoms of muscular disease. In most cases, it is diseases of the vascular or nervous system or problems with the processes providing energy within the muscle that are responsible for clinical problems with muscles. Other clinical problems include the muscular dystrophies, myotonic disorders, inflammatory myopathies and disorders of neuromuscular transmission (see Walton, 1996). The best known is Duchenne muscular dystrophy. 

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. 

A pathological rise in serum Mg levels also causes inhibition of ACh release, hence inhibition of neuromuscular transmission. 

Muscle relaxants cause a flaccid paralysis of skeletal musculature by binding to motor endplate cholinoceptors, thus blocking neuromuscular transmission (p. 

By preventing the binding of released ACh, it blocks neuromuscular transmission. Muscular paralysis develops within about 4 min. d-Tubocurarine does not penetrate into the CNS. The patient would thus experience motor paralysis and inability to breathe, while remaining fully conscious but incapable of ex-Ltillmann, Color Atlas of Pharmacology 2000 Thieme All rights reserved. Usage subject to terms and oonditlons of lloense. 

Duchenne muscular dystrophy yerapam may decrease neuromuscular transmission in patients with Duchenne muscular dystrophy and prolong recovery from the neuromuscular blocking agent vecuronium. Decrease in verapamil dosage may be necessary. 

Pharmacology Magnesium prevents or controls convulsions by blocking neuromuscular transmission and decreasing the amount of acetylcholine liberated by the motor nerve impulse. 

The effect of administering different botulinum neurotoxin serotypes at the same time or within several months of each other is unknown. Excessive neuromuscular weakness may be exacerbated by administration of another botulinum toxin prior to the resolution of the effects of a previously administered botulinum toxin. Aminoglycosides Cautiously perform coadministration of botulinum toxin type A and aminoglycosides or other agents interfering with neuromuscular transmission (eg, curare-like nondepolarizing blockers, lincosamides, polymyxins, quinidine, magnesium sulfate, anticholinesterases, succinylcholine chloride) because the effect of the toxin may be potentiated. 

In addition to the above-mentioned properties, the piperidine alkaloids exhibit a wide range of physiological activities. Thus, neuromuscular transmission is shown to be blocked by Ic and Id (72). Mitochondrial respiration is decreased and oxidative phosphorylation uncoupled at low concentrations of Ig (75), which, in addition to cw-6-methyl-2-(cw-6 - -pentadecenyl)piperidine (2c), inhibits the reactions of the Na+, K + -ATPase (14). 

Booij LH. Neuromuscular transmission and its pharmacological blockade. Part 2 Pharmacology of neuromuscular blocking agents. B Pharm World Sci 1997 19(1) 13-34. 

A young man broke his leg in a skiing accident, causing severe muscular spasm that necessitated relaxation of the muscle with a competitive nicotinic receptor antagonist before the fracture could be set. At the end of the orthopaedic procedure, the doctor restored neuromuscular transmission by administering ... 

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