Regeneration influences expression of the Na +,K +-ATPase subunit isoforms in the rat peripheral nervous system

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Abstract

Neural injury triggers changes in the expression of a large number of gene families. Particularly interesting are those encoding proteins involved in the generation, propagation or restoration of electric potentials. The expression of the Na +,K +-ATPase subunit isoforms (α, β and γ) was studied in dorsal root ganglion (DRG) and sciatic nerve of the rat in normal conditions, after axotomy and during regeneration. In normal DRG, α1 and α2 are expressed in the plasma membrane of all cell types, while there is no detectable signal for α3 in most DRG cells. After axotomy, α1 and α2 expression decreases evenly in all cells, while there is a remarkable onset in α3 expression, with a peak about day 3, which gradually disappears throughout regeneration (day 7). β1 Is restricted to the nuclear envelope and plasma membrane of neurons and satellite cells. Immediately after injury, β1 shows a homogeneous distribution in the soma of neurons. No β2 expression was found. β3 Specific immunofluorescence appears in all neurons, although it is brightest in the smallest, diminishing progressively after injury until day 3 and, thereafter, increasing in intensity, until it reaches normal levels. FXYD7 is expressed weakly in a few DRG neurons (less than 2%) and Schwann cells. It increases intensely in satellite cells immediately after axotomy, and in all cell types at day 3. Transient switching of members of the Na +,K +-ATPase isoform family elicited by axotomy suggests variations in the sodium pump isozymes with different affinities for Na +,K + and ATP from those in intact nerve. This adaptation may be important for regeneration. © 2004 IBRO. Published by Elsevier Ltd. All rights reserved.

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Arteaga, M. F., Gutiérrez, R., Avila, J., Mobasheri, A., Díaz-Flores, L., & Martín-Vasallo, P. (2004). Regeneration influences expression of the Na +,K +-ATPase subunit isoforms in the rat peripheral nervous system. Neuroscience, 129(3), 691–702. https://doi.org/10.1016/j.neuroscience.2004.08.041

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