In neuromuscular transmission

Myasthenia gravis is an autoimmune disease resulting from production of autoantibodies against AChR at the motor end plate, causing defects in neuromuscular transmission. Depending on the muscles affected a patient may develop dysphagia or respiratory failure [1]. The appearance of pathological forms of erythrocytes such as stomatocytes, echinocytes etc., in peripheral blood causes microcirculation disorders [2]. 

During the 16th century, European explorers found that natives in the Amazon Basin of South America were using curare, an arrow poison that produced skeletal muscle paralysis, to kill animals. The active compound, d-tubocurarine, and its modern synthetic derivatives, have had a major influence on the practice of anesthesia and surgery and have proved useful in understanding the basic mechanisms involved in neuromuscular transmission. 

At least two additional types of acetylcholine receptors are found within the neuromuscular apparatus. One type is located on the presynaptic motor axon terminal, and activation of these receptors mobilizes additional transmitter for subsequent release by moving more acetylcholine vesicles toward the synaptic membrane. The second type of receptor is found on perijunctional cells and is not normally involved in neuromuscular transmission. However, under certain conditions (eg, prolonged immobilization, thermal burns), these receptors may proliferate sufficiently to affect subsequent neuromuscular transmission. 

Myosmine (3[2-pyrrolidinyl]pyridine) and nicotine (3[l-methyl-2-pyrrolidinyl]pyridine) (Section 1, Appendix) and a number of related bioactive alkaloids occur in Nkotiana tabacum (tobacco) (Solanaceae) and variously in other Solanaceae such as Duboisia species. Nicotine and the related tobacco compounds nicotyrine and (—)-nornicotine are agonists (neurotransmitter mimics ) of the so-called (nicotine binding) nACh-R involved in neurotransmission and in neuromuscular transmission for skeletal muscle. The extraordinary addictiveness of nicotine derives from nACh-R agonists causing dopamine release and activating the mesolimbic dopamine system yielding reward effects. The antidepressant (—)-cotinine is the major nicotine metabolite in humans and a nicotinic agonist. 

In the rat, the 16S form is found in high concentration at the endplates and it is thought to be involved in neuromuscular transmission (Hall, 1973). The different molecular forms of AChE in SOL and EDL have apparent Km values similar to that previously foimd in the diaphragm muscle (Hall, 1973 Grosswald and Dettbam, 1983a, b). There appears to be no difference between catalytic sites of the molecular forms of AChE in fast EDL and slow SOL muscles, despite the different molecular form patterns and activity in three muscles. 

Fatigue (defined as a decline in force following repeated contractions) can occur as a result of a failure to activate motoneurons (commonly referred to as central fatigue) or from failiire in neuromuscular transmission, excitation-contraction coupling, or from the mismatching of energy... 

Not understood. For the partial reversal of neuromuscular blockade, one idea, based on animal studies, is that adrenocortical insufficiency causes a defect in neuromuscular transmission, which is reversed by the corticosteroids. Another idea is that the effects seen are connected in some way with the steroid nucleus of the pancuronium and vecuronium, and are mediated presynaptically. ... 

Potassium is involved in neuromuscular transmission and this is disturbed when the serum potassium is low. The results of this... 

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