This may explain why withdrawal of neuromuscular blocking agents sometimes is fatal to patients who have been on respirators. And it supports the idea that learning involves rapid molecular changes at cellular junctions in the brain. Lichtman is a professor of neurobiology at Washington University School of Medicine in St. Louis. He and his colleagues report their findings in the Oct. 15 issue of Science. Postdoctoral fellow Mohammed Akaaboune, Ph.D., is first author of the paper, which is accompanied by a commentary from Miriam M. Salpeter, Ph.D., of Cornell University.
Neuromuscular synapses connect nerve terminals to muscle fibers.
When the nerve terminal releases a chemical signal called acetylcholine, protein molecules on the muscle fiber's surface bind the acetylcholine and initiate a chain of events that lead to muscle contraction. These protein molecules, called acetylcholine receptors, huddle under the nerve terminal so they are in the best place to receive the chemical signal. For many years, Lichtman's group has used a fluorescent form of bungarotoxin to light up acetylcholine receptors in living animals. This constituent of snake venom permanently combines with the receptors, putting muscles out of action. In 1996, a researcher in Lichtman's lab, Stephen G. Turney, figured out how to use this labeling technique to measure the amount of acetylcholine receptor protein at individual synapses.