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Published May 19, 1977 | public
Journal Article

Two Mutations of Synaptic Transmission in Drosophila

Abstract

Evoked transmitter release is abnormal at the larval neuromuscular junctions of two Drosophila mutants. Following a single nerve impulse, the increased calcium conductance at the nerve terminal, which lasts for 1 ms in normal larvae, lasts for at least 60 ms in one mutant and several seconds in the other. Both mutations appear to affect the same gene on the X-chromosome. Normal larvae treated with 4-aminopyridine, a potassium channel blocking agent, mimic the abnormal synaptic transmission of one mutant. Normal larvae treated with tetraethylammonium, another potassium channel blocking agent, mimic the abnormal synaptic transmission of the other mutant. From these and other experiments, we suggest that the abnormal neuromuscular transmission in these mutants may be caused by defective potassium channels in the nerve terminal membrane.

Additional Information

© 1977 The Royal Society. Communicated by S. Benzer, For. Mem. R.S. - Received 22 November 1976. We thank Dr Seymour Benzer for advice, equipment, and mutants, and Drs James Hudspeth, Robert Mitchell and Felix Strumwasser for the use of equipment. We appreciate the helpful criticisms of this manuscript by Drs Seymour Benzer, Jac Sue Kehoe, Philippe Ascher, William Harris, William Quinn, Jr, Alain Ghysen, Duncan Byers, Donald Ready and Regis Kelly. This work was supported in part by Grant CB-27228 from the National Science Foundation to Seymour Benzer, Grant 1 ROI NS 10792 from the National Institutes of Health to Michael Dennis, a Scottish Rite Schizophrenia Research Program Grant and a postdoctoral fellowship from the Muscular Dystrophy Association to Yuh Nung Jan, as well as a postdoctoral fellowship from the National Institutes of Health to Lily Yeh Jan.

Additional details

Created:
August 19, 2023
Modified:
October 19, 2023