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The neuromuscular junction lies beyond the protective security network of the blood–brain barrier and the connective tissue sheaths of peripheral nerves. This makes it vulnerable to attack by a variety of foreign agents such as the bacterial toxin that causes botulism and the paralytic components of animal venoms such as α-latrotoxin, produced by the black widow spider. In addition, homology between foreign antigens and extracellular components of \`self' proteins (\`molecular mimicry') may result in autoantibodies of internal origin, arising during the normal defensive activity of the immune system, acting as double agents by binding to normal components of the neuromuscular junction. In the Miller–Fisher syndrome (MFS), a variant of Guillain–Barre syndrome characterized by ophthalmoplegia, areflexia and ataxia, it has been known for some time that antibodies against GQ1b gangliosides are generally present (reviewed in Willison and O'Hanlon, 1999) and that these antibodies can bind to motor nerve terminals and disrupt their function (Roberts et al ., 1994; Buchwald et al ., 1995). This has led to the suggestion that impairment of neuromuscular transmission may lie at the heart of some of the motor symptoms of MFS. In the present issue, O'Hanlon and colleagues take this evidence further with their report of overt structural breakdown of the nerve terminal associated with …

Double agents and breakdown of integrity at the neuromuscular junction in Miller-Fisher syndrome