Nerve Terminal Excitability and Neuromuscular Transmission in T(X;Y)V7 and Shaker Mutants of Drosophila Melanogaster

Abstract

We investigated the neuromuscular transmission in relation with genetic neuronal excitability changes in mutants T(X;Y)V7 and Sh^KS133 of Drosophila. These mutations affect two different genes belonging to the Shaker gene complex which encode different yet functionally related proteins. Experiments were performed on neuromuscular junctions from Drosophila larvae by recording pre- and postsynatic membrane currents using external electrodes. It was found that the neuromuscular electrophysiological phenotype of T(X;Y)V7 is caused by presynaptic membrane hyperexcitability probably in relation with a Ca²⁺-dependent down regulation of voltage dependent K channels. By contrast, the Sh^KS133 phenotype can be explained solely by action potential widening due to the absence of type-A K channels.

Key Words:

• Shaker mutants
• Shaker locus translocation
• larval neuromuscular junction
• membrane hyperexcitability
• type-A potassium channels
• potassium channels
• channel modulation
• presynaptic currents