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F‐actin distribution at nodes of Ranvier and Schmidt‐Lanterman incisures in mammalian sciatic nerves
Author(s) -
Kun Alejandra,
Canclini Lucía,
Rosso Gonzalo,
Bresque Mariana,
Romeo Carlos,
Hanusz Alicia,
Cal Karina,
Calliari Aldo,
Sotelo Silveira José,
Sotelo José R.
Publication year - 2012
Publication title -
cytoskeleton
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.95
H-Index - 86
eISSN - 1949-3592
pISSN - 1949-3584
DOI - 10.1002/cm.21011
Subject(s) - biology , actin cytoskeleton , cytoskeleton , microbiology and biotechnology , cytochalasin d , actin , sciatic nerve , anatomy , schwann cell , neuroscience , cell , biochemistry
Very little is known about the function of the F‐actin cytoskeleton in the regeneration and pathology of peripheral nerve fibers. The actin cytoskeleton has been associated with maintenance of tissue structure, transmission of traction and contraction forces, and an involvement in cell motility. Therefore, the state of the actin cytoskeleton strongly influences the mechanical properties of cells and intracellular transport therein. In this work, we analyze the distribution of F‐actin at Schmidt‐Lanterman Incisures (SLI) and nodes of Ranvier (NR) domains in normal, regenerating and pathologic Trembler J (TrJ/+) sciatic nerve fibers, of rats and mice. F‐actin was quantified and it was found increased in TrJ/+, both in SLI and NR. However, SLI and NR of regenerating rat sciatic nerve did not show significant differences in F‐actin, as compared with normal nerves. Cytochalasin‐D and Latrunculin‐A were used to disrupt the F‐actin network in normal and regenerating rat sciatic nerve fibers. Both drugs disrupt F‐actin, but in different ways. Cytochalasin‐D did not disrupt Schwann cell (SC) F‐actin at the NR. Latrunculin‐A did not disrupt F‐actin at the boundary region between SC and axon at the NR domain. We surmise that the rearrangement of F‐actin in neurological disorders, as presented here, is an important feature of TrJ/+ pathology as a Charcot‐Marie‐Tooth (CMT) model. © 2012 Wiley Periodicals, Inc

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