AbstractThe two‐electrode voltage clamp technique was employed to measure end‐plate currents in larval neuromuscular junctions of wild‐type (Canton‐S) and of three differentDrosophilaShaker mutants: ShakerKS133, Shaker102and f5Shaker5. 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 Ca2+channel blockers like Mg2+, at millimolar concentrations, and Co2+and Cd2+, at micromolar concentrations, but not by nifedipine (100 nM) and verapamil (100 nM). After exposure to Ca2+channel blockers, Shaker end‐plates exhibited PTP. In particular, Cd2+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 inDrosoph
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