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Shaker Mutants Lack Post‐tetanic Potentiation at Motor End‐plates
Author(s) -
Delgado Ricardo,
Latorre Ramon,
Labarca Pedro
Publication year - 1994
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1994.tb00614.x
Subject(s) - shaker , neuromuscular junction , 4 aminopyridine , long term potentiation , biophysics , chemistry , anatomy , potassium channel , biology , biochemistry , neuroscience , receptor , physics , quantum mechanics , vibration
The two‐electrode voltage clamp technique was employed to measure end‐plate currents in larval neuromuscular junctions of wild‐type (Canton‐S) and of three different Drosophila Shaker mutants: Shaker KS133 , Shaker 102 and f 5 Shaker 5 . In the Shaker mutants, nerve‐evoked end‐plate currents (neepc) were 4–5‐fold larger than those measured in Canton‐S. Shaker motor end‐plates were found to lack post‐tetanic potentiation (PTP), but could undergo facilitation. Moreover, PTP but not facilitation was lost in wild‐type larvae if the neuromuscular junction was exposed to 4‐aminopyridine (4‐AP), a blocker of Shaker A‐type K + currents. End‐plate currents were depressed by Ca 2+ channel blockers like Mg 2+ , at millimolar concentrations, and Co 2+ and Cd 2+ , at micromolar concentrations, but not by nifedipine (100 nM) and verapamil (100 nM). After exposure to Ca 2+ channel blockers, Shaker end‐plates exhibited PTP. In particular, Cd 2+ was most effective in depressing neepes and in restoring PTP in all Shaker mutants. The results obtained indicate the abnormal function of Shaker K + channels at motor nerves specifically abolishes PTP in Drosophila larval neuromuscular junctions.