Decreased transmitter release conferred by a mutation in the slowpoke-encoded calcium-dependent potassium channel gene at the Drosophila neuromuscular junction

Using immunocytochemical and electrophysiological methods, the effects of mutations in the structural gene for a calcium activated potassium channel, slowpoke (slo), in Drosophila melanogaster were studied. Anti-horseradish peroxidase was used to visualize the branching of the nerves innervating the body wall muscles. No differences are observed between slo and normal larvae. Defects in synaptic transmission at the neuromuscular junction were analyzed electrophysiologically. slo mutants show significant reductions in transmitter release. Also, slo mutations paired with hyperexcitable mutants (Shaker, ether a go go) and/or pharmacological agents (4-aminopyridine) significantly decrease the high amounts of transmitter release normally observed in these situations. Significant reductions in transmitter release caused by the slo mutation are only observed at low external calcium concentrations. This decrease in transmitter release may be due to reduced neuronal excitability conferred by the slo mutation