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- W1980072629 abstract "Axons degenerate after injury and in neuropathies and disease via a self-destruction program whose mechanism is poorly understood. Axons that have lost connection to their cell bodies have altered electrical and synaptic activities, but whether such changes play a role in the axonal degeneration process is not clear. We have used a Drosophila model to study the Wallerian degeneration of motoneuron axons and their neuromuscular junction synapses. We found that degeneration of the distal nerve stump after a nerve crush is greatly delayed when there is increased potassium channel activity (by overexpression of two different potassium channels, Kir2.1 and dORKΔ-C) or decreased voltage-gated sodium channel activity (using mutations in the para sodium channel). Conversely, degeneration is accelerated when potassium channel activity is decreased (by expressing a dominant-negative mutation of Shaker). Despite the effect of altering voltage-gated sodium and potassium channel activity, recordings made after nerve crush demonstrated that the distal stump does not fire action potentials. Rather, a variety of lines of evidence suggest that the sodium and potassium channels manifest their effects upon degeneration through changes in the resting membrane potential, which in turn regulates the level of intracellular free calcium within the isolated distal axon." @default.
- W1980072629 created "2016-06-24" @default.
- W1980072629 creator A5013006072 @default.
- W1980072629 creator A5017035439 @default.
- W1980072629 creator A5049219339 @default.
- W1980072629 creator A5089766115 @default.
- W1980072629 date "2013-11-27" @default.
- W1980072629 modified "2023-10-16" @default.
- W1980072629 title "Sodium and Potassium Currents Influence Wallerian Degeneration of Injured Drosophila Axons" @default.
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- W1980072629 doi "https://doi.org/10.1523/jneurosci.1007-13.2013" @default.
- W1980072629 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3841444" @default.
- W1980072629 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24285879" @default.
- W1980072629 hasPublicationYear "2013" @default.
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