Dysferlin deficient mouse muscle fibers fail to perform calcium-dependent membrane resealing [ 6], a process thought to involve fusion and exocytosis [ 7, 8] or endocytosis [ 9] of repair vesicles at sites of injury.
Molecular transfer of small molecules (<4 kDa) across the permeabilized area of the membrane is mostly driven by the concentration gradient across the membrane described by the Fick equation during the resealing process, i.e., after the pulse delivery [ 32] (Fig. 1).
Most likely, the influx of Ca2+ is required for membrane resealing, which is common in wound repair processes in other organisms (Bement et al., 1999; Steinhardt et al., 1994; Togo et al., 1999).
This resealing process is not just due to the viscoelasticity of the membrane, but occurs through defect patching mediated by exocytotic pathways [ 27].
It is known that intracellular calcium is a key factor that is essential to membrane resealing.
Furthermore, 1 μM BayK 8644, a VDCC agonist, significantly enhanced membrane resealing.
These data suggest that VDCC play a critical role in membrane resealing.
Further, there is likely an appropriate range of calcium influx through VDCC which ensures effective axonal membrane resealing.
Membrane resealing was assessed by the changes of membrane potential and compound action potential (CAP), and exclusion of horseradish peroxidase 60 min following trauma.
The design of effective electroporation protocols for molecular delivery applications requires the determination of transport parameters including diffusion coefficient, membrane resealing, and critical electric field strength for electroporation.
