By Matthew N. Meriggioli
This source covers all facets of the analysis and scientific administration of sufferers with ailments of the neuromuscular junction. It breaks down each one disorder by way of pathophysiology, medical presentation and traditional heritage and direction for superior prognosis and remedy.
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Additional info for Neuromuscular Junction Disorders: Diagnosis and Treatment (Neurological Disease and Therapy)
Sample text
J Physiol (Lond) 1992; 458:85–97. Flucher BE, Daniels MP. Distribution of Na+ channels and ankyrin in neuromuscular junctions is complementary to that of acetylcholine receptors and the 43 kD protein. Neuron 1989; 3:163–175. Ruff RL, Whittlesey D. Na+ currents near and away from endplates on human fast and slow twitch muscle fibers. Muscle Nerve 1993; 16:922–929. Lindstrom JM. Acetylcholine receptors and myasthenia. Muscle Nerve 2000; 23:453–477. Mishina M, Taki T, Imoto K, Noda M, Takahashi T, Numa S, Methfessl C, Sakmann B.
The decrease in quantal content persists as long as low-frequency stimulation is continued. After cessation of stimuli, a short period of time (20–30 s) is required for the mobilization process to restore the readily releasable pool of vesicles to the resting level. It is helpful to keep in mind that the above processes occur in normal muscle. Thus, under normal circumstances, the additional calcium in the nerve terminal caused by high-frequency stimulation (posttetanic facilitation) is clinically inconsequential since the quantal content is always more than sufficient to result in a single muscle action potential.
Land BR, Salpeter EE, Salpeter MM. Kinetic parameters for acetylcholine interaction in intact neuromuscular junction. Proc Natl Acad Sci USA 1981; 78:7200–7204. Ruff RL, Whittlesey D. Na+ current densities and voltage dependence in human intercostals muscle fibres. J Physiol (Lond) 1992; 458:85–97. Flucher BE, Daniels MP. Distribution of Na+ channels and ankyrin in neuromuscular junctions is complementary to that of acetylcholine receptors and the 43 kD protein. Neuron 1989; 3:163–175. Ruff RL, Whittlesey D.