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Journal of Neuroscience, Vol 11, 3257-3267, Copyright © 1991 by Society for Neuroscience
Membrane resealing in cultured rat septal neurons after neurite transection: evidence for enhancement by Ca(2+)-triggered protease activity and cytoskeletal disassembly
XY Xie and JN Barrett
Department of Physiology and Biophysics, University of Miami School of Medicine, Florida 33101.
Neurites of cultured septal neurons were transected with a laser under
sterile conditions, and the subsequent membrane resealing was assayed using
a dye exclusion method. In agreement with findings in other preparations,
Ca2+ enhanced resealing: in normal culture medium the percentage of
lesioned neurons that resealed within 20-30 min after transection increased
with increasing bath [Ca2+] over the range 10(-7) to 2 x 10(-3) M; about
75% of cells resealed in 2 mM Ca2+. Mn2+ and Sr2+ also enhanced resealing,
but Mg2+ inhibited it. The percentage of resealing neurons was sensitive to
agents known to alter the stability of cytoskeletal components. Agents that
tend to disassemble microtubules and/or neurofilaments (e.g., colchicine,
low-ionic- strength media) strongly promoted resealing, whereas treatments
that tend to stabilize microtubules (taxol, Mg2+) inhibited resealing.
Addition of exogenous proteases (papain, trypsin, or dispase) enhanced
resealing, whereas inhibitors of cysteine proteases (including a specific
inhibitor of calpain, a Ca-activated neutral protease) strongly inhibited
resealing. Calmodulin inhibitors inhibited resealing, consistent with
reports that calmodulin facilitates calpain- mediated proteolysis of
fodrin, a component of the cortical cytoskeleton. Based on these results,
we hypothesize that one of the major mechanisms involved in resealing is
activation of endogenous proteases by Ca2+ entry into the injured neurite.
The resulting changes in the cellular cytoskeleton might promote fusion and
resealing of the cut ends of the plasma membrane by enhancing membrane
mobility and/or by removing structures that normally prevent
membrane-membrane contact.
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