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Published January 1978 | Published
Journal Article Open

Genetic dissection of short-term and long-term facilitation at the Drosophila neuromuscular junction

Abstract

Transmitter release at the Drosophila larval neuromuscular junction may be increased by previous activity of the nerve. This facilitation phenomenon involves at least two processes, one short-term and the other long-term. These are shown to be based on different mechanisms because (i) a mutant was found that had abnormal long-term facilitation but normal short-term facilitation; and (ii) long-term facilitation was eliminated by tetrodotoxin or by removing external Na+ but short-term facilitation was not. In long-term facilitation, there was a prolonged release of transmitter due to a prolonged Ca2+ sensitivity of the presynaptic terminal after each nerve stimulus. The cause of this is probably accumulation of Na+ inside the nerve terminal.

Additional Information

© 1978 by the National Academy of Sciences. Communicated by Seymour Benzer, October 17, 1977. We thank Dr. Seymour Benzer for advice, equipment, and mutant. We appreciate the helpful criticisms of this manuscript by many, especially Drs. Seymour Benzer, Stephen Kuffler, Michael Dennis, A.R. Martin, and William Harris. This work was supported in part by Grant GB-27228 from the National Science Foundation to Seymour Benzer, a postdoctoral fellowship from the Muscular Dystrophy Association to Y.N.J., and a postdoctoral fellowship from the National Institutes of Health to L.Y.J. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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August 22, 2023
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