Nerve terminal excitability and neuromuscular transmission in T(X;Y)V7 and Shaker mutants of Drosophila melanogaster.
We investigated the neuromuscular transmission in relation with genetic neuronal excitability changes in mutants T(X;Y)V7 and ShK,S133 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 postsynaptic 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 ShKS133 phenotype can be explained solely by action potential widening due to the absence of type-A K channels.
Mallart
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A
Unité de Physiologie Neuromusculaire, CNRS, Gif Sur Yvette, France.
Angaut-Petit
D
D
Bourret-Poulain
C
C
Ferrús
A
A
D000818:Animals; D002118:Calcium / Q000378:metabolism; D004331:Drosophila melanogaster / Q000235:genetics* / Q000502:physiology; D015640:Ion Channel Gating; D007814:Larva / Q000502:physiology; D008564:Membrane Potentials; D009154:Mutation; D009431:Neural Conduction / Q000502:physiology; D009469:Neuromuscular Junction / Q000502:physiology*; D015221:Potassium Channels; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*
D015221:Potassium Channels; D002118:Calcium