|Citation||Hodges, D.D., Lee, D., Preston, C.F., Boswell, K., Hall, L.M., O'Dowd, D.K. (2002). tipE regulates Na[+]-dependent repetitive firing in Drosophila neurons. Mol. Cell. Neurosci. 19(3): 402--416. (Export to RIS)|
|Publication Type||Research paper|
|PubMed Abstract||The tipE gene, originally identified by a temperature-sensitive paralytic mutation in Drosophila, encodes a transmembrane protein that dramatically influences sodium channel expression in Xenopus oocytes. There is evidence that tipE also modulates sodium channel expression in the fly; however, its role in regulating neuronal excitability remains unclear. Here we report that the majority of neurons in both wild-type and tipE mutant (tipE-) embryo cultures fire sodium-dependent action potentials in response to depolarizing current injection. However, the percentage of tipE- neurons capable of firing repetitively during a sustained depolarization is significantly reduced. Expression of a tipE+ transgene, in tipE- neurons, restores repetitive firing to wild-type levels. Analysis of underlying currents reveals a slower rate of repolarization-dependent recovery of voltage-gated sodium currents during repeated activation in tipE- neurons. This phenotype is also rescued by expression of the tipE+ transgene. These data demonstrate that tipE regulates sodium-dependent repetitive firing and recovery of sodium currents during repeated activation. Furthermore, the duration of the interstimulus interval necessary to fire a second full-sized action potential is significantly longer in single- versus multiple-spiking transgenic neurons, suggesting that a slow rate of recovery of sodium currents contributes to the decrease in repetitive firing in tipE- neurons.|
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|Language of Publication||English|
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|Abbreviation||Mol. Cell. Neurosci.|
|Title||Molecular and Cellular Neurosciences|
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