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Barrier permeability at cut axonal ends progressively decreases until an ionic seal is formed
C S Eddleman1, G D Bittner, H M Fishman
1Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston, Texas 77555-0641, USA.
Biophysical Journal
|October 12, 2000
Summary
Axonal injury triggers a gradual barrier formation at cut ends, restricting molecule entry over time. This process, involving vesicles, eventually seals the axon, restoring normal electrical function.
Area of Science:
- Neuroscience
- Cell Biology
- Biophysics
Background:
- Axonal severance triggers rapid barrier formation at cut ends to limit molecular exchange.
- Understanding the kinetics and mechanisms of this barrier is crucial for nerve regeneration research.
Purpose of the Study:
- To determine the time course of barrier formation after axonal severance in crayfish.
- To investigate the relationship between molecular size and barrier permeability.
- To elucidate the mechanism of axolemmal sealing.
Main Methods:
- Utilized hydrophilic fluorescent dyes of varying molecular sizes (0.6-70 kDa) to assess barrier permeability.
- Measured the temporal decline of ionic injury currents.
- Confirmed axolemmal ionic seal formation by monitoring resting and action potentials.
- Employed confocal microscopy to visualize dye exclusion and barrier development.
Main Results:
- Dye exclusion time correlated inversely with molecular size, indicating a size-dependent barrier.
- A barrier to small molecules formed within 60 minutes, while ionic seal formation took longer (>60 minutes).
- Axolemmal sealing occurred gradually, not suddenly, involving accumulating and interacting injury-induced vesicles.
Conclusions:
- Axonal barrier formation is a slow, progressive process, not an abrupt event.
- The gradual restriction of molecules of progressively smaller size leads to the eventual axolemmal ionic seal.
- Complete ionic seal formation is indicated by the return of ionic injury current to baseline levels.