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that generate antibodies to AChR in culture T lymphocytes speci c to AChRs are also found in patients with myasthenia207,452,521,522 The following is an event sequence proposed in an attempt to explain both the initiation and the maintenance of MG Macrophages and dendritic cells activated for as of yet unknown reasons act as an antigenpresenting cell16,18,230,231,233,523 This macrophage may phagocytize and degrade AChRs into peptide subcomponents, which are then linked with a class II major histocompatibility complex (MHC; eg, HLA-B8, DR3, and DQw2), the molecule required for reactivity to self-antigens 524 This AChR antigenic fragment and MHC complex are transported to the macrophage s and dendritic cells surface There, speci c helper T cells, in cooperation with the CD3 complex and CD4 molecular T-cell receptor site, recognize this antigenic complex525 529 Additionally, speci c receptor sites on the T cells recognize cytokines secreted by the macrophage and dendritic cells The activated helper T cells begin to secrete substances, which act to stimulate speci c B lymphocytes The activated B lymphocytes grow and differentiate into plasma cells These differentiated plasma cells manufacture IgG anti-AChR antibodies that bind to NMJ AChRs These AChR antibodies are polyclonal, including multiple IgG subclasses directed at different but speci c sites on the AChR111,123,529 532 There are a number of mechanisms by which antibodies adversely affect NMT This includes not only a decreased number of AChRs as described below, but also a diminished postsynaptic membrane area associated with fewer postjunctional folds and, as a result, increased synaptic space180 182,418,419 421 A number of antibodies belonging to the IgG class are directed against the main immunogenic receptor as well as other sites on the AChR (Fig 23 5)122,533 535 Once bound to the AChR, these antibodies initiate a number of irreversible processes, all of which are directed at the AChR and postsynaptic membrane In addition to the complementmediated AChR destruction, the antibodies, by binding to a nearby site, may physically block the ACh-binding site by steric hindrance536 It is also possible that antibody binding may prevent the necessary conformational change required to open the ion pore The antibodies not only bind to the AChR but also cross-link with other antibodies537,538 When the AChRs are cross-linked in this manner, these are reabsorbed by the postsynaptic membrane by a process known as endocytosis This degradation process occurs up to three times faster than unlinked AChRs The AChR population is diminished as a result539 541 The normal NMJ AChR half-life of 5 10 days is dramatically reduced539,540,542 Synthesis of new AChRs remains unchanged, thus resulting in the net reduction of total AChRs per NMJ.

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The MMC is a shell program that holds individual utilities called snap-ins The rst time you create an MMC, you get a default blank console A blank MMC isn t much to look at like any new toolbox, it starts out empty Step 1 To create your MMC, select Start | Run, type mmc, and then click OK Voil ! You ve created a blank console (Figure 13-18) Notice that the name in the upper-left corner is Console 1 Before you actually con gure an MMC, you need to understand a few points First, you can have more than one MMC; successive consoles will be given default names such as Console 2, Console 3, and so on Second, you can rename the consoles that you create and choose where to save them so that you can easily nd them again Finally, once you ve created an MMC, you can modify it by adding or taking away tools just like your toolbox at home Follow these steps to practice working with MMCs: a) Click File (Windows XP) or Console (Windows 2000) | Save As and ll in the boxes as follows:

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Finally, the antibodies are believed to result in activation of the complement cascade that is directed at the postsynaptic membrane165 167,172,173,180 182,543,544,545 Destruction of the postsynaptic membrane has several adverse consequences Simpli cation of the postsynaptic membrane reduces the surface area available for AChRs Widening of the synaptic cleft has the effect of increasing the diffusion time of ACh from the pre- to postsynaptic membranes, thus increasing ACh s exposure to AChE All these factors act in concert to reduce the NMJ s safety factor by reducing the probability of ACh AChR interaction Less ACh will get to the receptor (longer diffusion times, increased exposure to AChE, and greater chance to diffuse out of the synaptic space), and fewer AChRs will be available and responsive to the ACh that eventually arrives Regardless of mechanism, impaired ACh binding renders the AChRs whose numbers are reduced or function impaired unable to contribute in a normal fashion to the generation of an EPP The reduced number of activated AChRs per unit region of postsynaptic membrane translates into a reduction of EPP amplitude In addition to its primary effects of the AChR channel, MG also reduces the EPP by affecting the number of end-plate voltage-gated sodium channels546 Support for the above hypotheses in MG is provided by (1) the documentation of IgG complexed with AChRs, (2) identi cation of IgG localized to the postsynaptic membrane,180 182,420 (3) circulating IgG antibodies that are found in over 90% of patients with MG,420 and (4) approximately 70 90% reduction in the total numbers of AChRs identi able at the postsynaptic membrane547 Puri ed immunoglobulins from patients with not only seropositive but also seronegative MG reversibly block currents through nicotinic AChR in patchclamp experiments548 In normal muscle tissue, it is possible to block approximately 75% of functioning AChRs and reduce EPP currents by only 60% of their normal amplitude, with maintenance of essentially normal NMJ transmission476,549,550 In MG, however, the con uence of all of the aforementioned factors means that blocking only a small number of the remaining AChRs is all that is required to transform a marginally functioning NMJ into one that is no longer capable of generating a muscle ber action potential and myo ber contraction A cause and effect relationship between anti-MuSK antibodies and MG is based, in large part, on their apparent speci city for patients with myasthenic phenotypes To date, there are at best modest morphological and electrophysiological data to support a direct role of anti-MuSK antibodies in the pathogenesis of MG MuSK knockout mice develop normally in utero but die perinatally with a virtual absence of postsynaptic differentiation551 Experimental MG has been produced.

in mice by immunization with one MuSK component In one patient who underwent an intercostal muscle biopsy, in vitro electrophysiology did disclose reduced MEPP amplitudes424 The pathophysiology of transient neonatal myasthenia results from the passive transplacental transfer of the mother s IgG AChR antibodies The reason why this disorder does not happen with greater frequency is unknown The pathophysiology and the genetics of familial limb-girdle MG are unknown It is presumed to be a postsynaptic disorder in view of its electrophysiological behavior

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