Slowpoke Speeds Repolarization at Fly Synaptic Terminals

Voltage-sensitive K channels speed membrane repolarization, thus narrowing action potential (AP) waveforms. The spike waveform at synaptic terminals strongly influences the kinetics of neurotransmitter release. Because recording APs at synaptic terminals is difficult, however, researchers typically examine EPSPs to identify contributors to presynaptic waveform. For example, mutation of shaker, which encodes a KV1-type channel, enlarges EJPs at Drosophila neuromuscular junctions, suggesting shaker contributes to membrane repolarization in presynaptic terminals. Mutation of slowpoke, encoding a Ca-activated K channel, does not significantly change EJPs, but it enhances the effect of shaker mutations. To directly assess the effects of these channels, Ford and Davis expressed a voltage-sensitive fluorescent protein in motor neurons. Supporting previous conclusions, loss of shaker widened presynaptic APs at low extracellular Ca concentrations. But previously undetected small depolarizations (“spikeletts”) occurred during membrane repolarization in shaker-null terminals. Waveform widening and spikeletts disappeared at physiological Ca concentration, but reappeared when slowpoke function was disrupted in shaker mutants, indicating that slowpoke contributes to AP repolarization under physiological conditions. F Development/Plasticity/Repair Schwann Cells Provide Directional Cues for Regenerating Axons