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Vesicle release also occurs in a singular and spontaneous fashion, unrelated to a nerve action potential stimulus This occurs at a frequency of about 02 003 times per second, resulting in the activation of 1 2 103 AChR channels and the generation of a nonpropagated MEPP with a magnitude of 05 1 mV358,498 The EPP amplitude generated by a nerve action potential is dependent on the number of quanta released and the amplitude of each MEPP The latter is determined by the number of ACh molecules per vesicle, and indirectly to the ef ciency by which ACh can be resynthesized and repackaged Measuring the content, number, and frequency of MEPP with in vitro recordings of myoneural junctions has provided many of the seminal insights regarding the pathophysiology of both acquired and inherited DNMT The half-life of an AChR in the junctional membrane is about 8 10 days499 This rapid turnover is a major reason why DNMT are more treatment responsive than other neuromuscular disorders where damaged components heal more slowly or incompletely The old receptors are internalized by the process of endocytosis and transported to lysosomes for degradation through an intricate network of intracellular tubules The AChR are not recycled but are replaced by newly synthesized receptors The cross-linking of the AChR by antibodies in patients with MG accelerates the internalization of the receptors and shortens their half-life, as described below Ultimately, effective NMT is dependent on a series of events, each of which is a potential rate-limiting factor ACh must be resynthesized and repackaged in a timely fashion into vesicles that need to be positioned to release themselves with suf cient numbers in response to a nerve action potential This process is facilitated by the ingress of calcium as well as the existence of a number of nerve terminal (SNARE) proteins, which promote the fusion of vesicles with, and subsequent release through, the presynaptic membrane This quantal release must then negotiate the synaptic cleft without either the inadequate or the excessive in uence of AChE, to bind with an adequate number of correctly positioned and functioning AChR In turn, these AChR must interact with Nav14 sodium channels, which have the same characteristics described as their AChR counterparts If all of this proceeds without a hitch, a muscle EPP suf cient to trigger a muscle ber action potential will occur in response to each and every stimulus in each and every muscle ber Both the anatomy and the physiology of NMT are codependent on the distal motor nerve terminal Schwann cells produce proteins such as neuregulins, nerve growth factors, and calcitonin gene-related protein that are capable of inducing AChR gene transcription in nearby muscle bers and are necessary for motor neuron survival and growth1,443 Neuregulins are yet another group of proteins that contribute to the clustering of AchR at the NMJ.

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For details on working with the MMC, refer to the Microsoft Management Console section in 13 of Mike Meyers A+ Guide to Managing and Troubleshooting PCs

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A small region of the muscle bers sarcoplasm, the junctional sarcoplasm, overlies the myo brils and extends into the junctional folds500 Clusters of ve to 10 myonuclei are also found here and serve the purpose of coding messenger RNA for the construction of AChRs501 503 The junctional sarcoplasm s function is to manufacture and degrade AChRs, to maintain an appropriate ionic balance for the sacroplasmic constituents, and to synthesize AChE for the synaptic space Temperature is an important clinical and electrophysiological consideration in NMT In patients with MG, a reduction in muscle temperature results in a number of well-documented ndings19,20,24,25,353 355,504,505 The magnitude of a decremental response during repetitive stimulation at a muscle temperature of 34 C can be signi cantly reduced or repaired by cooling muscle by only a few degrees The exact mechanism(s) of the diseased NMJ s response to alterations in temperature is only partially understood The duration and amplitude of the nerve action potential at the presynaptic terminal are increased by cooling203,506,507 This may result in prolongation of the calcium channels open time and subsequent augmentation of ACh release359,497,508 510 In addition, NMT is enhanced at cooler temperatures as the hydrolytic capability of AChE is signi cantly reduced at temperatures below 34 C, with an increased probability of ACh AChR interaction477 Reducing the affected muscle s temperature is known to increase the AChR s open time as well479 Finally, a reduction in muscle temperature leads to a lowering of the resting membrane potential, bringing it closer to threshold, thus requiring less of a stimulus for a single muscle ber action potential to take place These four factors and perhaps others as well serve to improve NMT in response to cooling and to potentially result in a false-negative EDX conclusion if the tested muscle is not adequately warmed Temperature-dependent changes in jitter can also be seen in persons with normal or abnormal NMJs with differing responses21,273 Jitter is <50 microseconds in persons with no known neuromuscular disease and is dependent on patient age and muscle selected Lowering the intramuscular temperature several degrees below 35 C increases jitter by 2 3 microseconds per degree, while further decreases in temperature toward 30 C result in a increase of jitter values by 6 8 microseconds per degree change In other words, the jitter increases from 50 to 60 70 microseconds and may even reach 100 microseconds at the temperature of 25 C270 The EPP s increased rise time and variability of all the factors necessary to facilitate ACh release may explain this Conversely, in patients with DNMT of any type but particularly those of the postsynaptic membrane, the jitter may actually improve with a reduction in muscle temperature Additionally, block present at 34 C may no longer occur at an intramuscular temperature of 30 C At reduced temperatures in patients with markedly abnormal.

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