Abstract
Axons of neurons are contractile, i.e., they actively maintain a rest tension. However, the spatial origin of this contractility along the axon and the role of the cytoskeleton in generating tension and sustaining rigidity are unknown. Here, using a microfluidic platform, we exposed a small segment of the axons of embryonic Drosophila motor neurons to specific cytoskeletal disruption drugs. We observed that a local actomyosin disruption led to a total loss in axonal tension, with the stiffness of the axon remaining unchanged. A local disruption of microtubules led to a local reduction in bending stiffness, while tension remained unchanged. These observations demonstrated that contractile forces are generated and transferred along the entire length of the axon in a serial fashion. Thus, a local force disruption results in a collapse of tension of the entire axon. This mechanism potentially provides a pathway for rapid tension regulation to facilitate physiological processes that are influenced by axonal tension.
Original language | English (US) |
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Pages (from-to) | 3133-3139 |
Number of pages | 7 |
Journal | Lab on a chip |
Volume | 19 |
Issue number | 18 |
DOIs | |
State | Published - Sep 21 2019 |
ASJC Scopus subject areas
- Bioengineering
- Biochemistry
- General Chemistry
- Biomedical Engineering