Neuromuscular Junction Disorders: Diagnosis and Treatment by Matthew N. Meriggioli

By Matthew N. Meriggioli

This source covers all points of the analysis and scientific administration of sufferers with illnesses of the neuromuscular junction. It breaks down each one disorder through pathophysiology, scientific presentation and traditional background and path for superior analysis and therapy.

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The mean probability of quantal release was normal or low, and the mean MEPP frequency was not significantly different compared to controls. However, the quantal store was decreased, and the mean probability of quantal store mobilization was high. Histologic evidence of denervation and small or absent nerve terminals were observed in all patients. Only a few of these endplates were innervated by regenerating nerve fibers. Failure of electrical stimulation to generate EPPs was observed and was frequency dependent, increasing with higher rates of stimulation.

Thus, with high-frequency stimulation, the nerve terminals are rapidly depleted of available ACh stores, likely underlying the frequent clinical complaint of muscle fatigue in these patients. As we have seen, high-frequency nerve stimulation enhances release of ACh due to build-up of calcium in the nerve terminal. This effectively coun- Pathophysiology of Neuromuscular Junction Disorders 41 ters the effect of stimulation-induced vesicle depletion in normal nerve terminals. However, an increase in nerve terminal calcium concentrations also increases mobilization of vesicles and their exocytosis.

Proteins of synaptic vesicles involved in exocytosis and membrane recycling. Neuron 1991; 6:665–677. Whittaker VP. The structure and function of cholinergic synaptic vesicles. Biochem Soc Trans 1984; 12:561–576. Perin MS, Fried VA, Mignery G, Jahn R, Sudhof TC. Phospholipid binding by a specific synaptic vesicle protein homologous to the regulatory region of protein kinase C. Nature 1990; 345:260–263. Sheng Z-H, Westenbroek RE, Catterall WA. Physical link and functional coupling of presynaptic calcium channels and the synaptic docking/fusion machinery.

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