Researchers at the University of Texas (Austin, USA) studied the mechanisms animal cells use to repair damage to their membranes and focused on invertebrates, which have a superior ability to regenerate nerve axons; this is due to the fact that invertebrate nerve axons not degenerate within days, as happens with mammals, but can survive for months, or even years. The severed proximal nerve axon in invertebrates can also reconnect with its surviving distal nerve axon to produce much quicker and much better restoration of behavior than occurs in mammals. The researchers then developed appropriate polyethylene glycol (PEG)-sealing protocols to repair cut- and crush-severed nerves in a rat model.

The procedure involves three stages. First, severed axonal ends are opened, and resealing is prevented by hypotonic Ca(2+) -free saline containing antioxidants that inhibit plasmalemmal sealing. Then, a hypotonic solution of PEG is applied to open closely apposed axonal ends to induce their membranes to flow rapidly into each other (PEG-fusion), consistent with data showing that PEG rapidly seals transected neurites independently of any known endogenous sealing mechanism. Third, Ca(2+) -containing isotonic saline is applied to induce sealing of any remaining plasmalemmal holes by inducing accumulation and fusion of vesicles. Two studies describing the procedure were published in the February 3, 2012, issue of the Journal of Neuroscience Research.

“Severed invertebrate nerve axons can reconnect proximal and distal ends of severed nerve axons within seven days, allowing a rate of behavioral recovery that is far superior to mammals,” said lead author Professor George Bittner, PhD. “In mammals the severed distal axonal stump degenerates within three days and it can take nerve growths from proximal axonal stumps months or years to regenerate and restore use of muscles or sensory areas, often with less accuracy and with much less function being restored.”

“We used rats as an experimental model to demonstrate how severed nerve axons can be repaired. Without our procedure, the return of nearly full function rarely comes close to happening,” added Prof. Bitnner. “This new approach to repairing nerve axons could almost-certainly be just as successful in humans.”

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