Logo image
Back
Microtubule reconfiguration during axonal retraction induced by nitric oxide
Journal article   Open access   Peer reviewed

Microtubule reconfiguration during axonal retraction induced by nitric oxide

Yan He, Wenqian Yu and Peter W Baas
The Journal of neuroscience, v 22(14), pp 5982-5991
15 Jul 2002
DOI: https://doi.org/10.1523/JNEUROSCI.22-14-05982.2002
PMID: 12122060
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://doi.org/10.1523/JNEUROSCI.22-14-05982.2002View
Published, Version of Record (VoR) Open

Abstract

Paclitaxel - pharmacology Nitric Oxide - pharmacology Nocodazole - pharmacology Ganglia, Spinal - cytology Microtubules - metabolism Tubulin - metabolism Neurons - ultrastructure Microtubules - drug effects Axons - ultrastructure Microtubules - ultrastructure Antineoplastic Agents - pharmacology Neurons - metabolism Nitric Oxide Donors - pharmacology Neurons - drug effects Hydrazines - pharmacology Ganglia, Spinal - embryology Cells, Cultured Axons - drug effects Axons - metabolism Cytoskeleton - ultrastructure Chick Embryo Tyrosine - metabolism Animals Cytoskeleton - metabolism Cytoskeleton - drug effects Microscopy, Fluorescence
Axonal retraction is induced by different types of physiological cues and is responsible for the elimination of mistargeted axons. There is broad agreement that alterations in the cytoskeleton underlie axonal retraction. The prevailing view is that axonal retraction involves a wholesale depolymerization of microtubules and microfilaments. However, axons retracting physiologically display a very different morphology than axons induced to retract by experimental depolymerization of microtubules. Experimental depolymerization of microfilaments actually prevents retraction rather than causing it. We have proposed an alternative hypothesis, namely that axonal retraction involves a backward retreat of cytoskeletal elements rather than their wholesale depolymerization. In the present study, we sought to test this hypothesis with regard to microtubules. When a donor of nitric oxide was applied to cultured chick sensory neurons, the majority of axons retracted dramatically within 30-60 min. Retracting axons were characterized by an enlarged distal region, a thin trailing remnant, and sinusoidal bends along the shaft. Quantitative immunofluorescence analyses showed no detectable loss of microtubule mass during retraction, even with regard to the most labile microtubules. Instead, microtubules were reconfigured into coiling and sinusoidal bundles to accommodate the shortening of the axon. Stabilization of microtubules by taxol did not prevent the retraction, even at concentrations of the drug that actually caused microtubule levels to increase. The retractions induced by nitric oxide were remarkably similar to those observed when motor proteins are manipulated, suggesting that these retractions may result from alterations in the activities of the motors that configure microtubules.

Metrics

4 Record Views
75 citations in Web of Science
76 citations in Scopus

Details

UN Sustainable Development Goals (SDGs)

This publication has contributed to the advancement of the following goals:

#3 Good Health and Well-Being

InCites Highlights

Data related to this publication, from InCites Benchmarking & Analytics tool:

Web of Science research areas
Neurosciences
Logo image