Axonal lipid bilayer at severed peripheral nerve ends

The axonal lipid bilayer at severed peripheral nerve ends is the primary physical substrate for PEG-fusion, a therapeutic technique designed to rapidly restore nerve continuity after traumatic injury (Bittner et al., 2016). In a typical nerve transection, the axonal membrane (axolemma) seals at the site of injury, which triggers Wallerian degeneration of the distal nerve segment and necessitates a slow, often incomplete, natural regeneration process. By targeting the lipid bilayers of the severed ends with a chemical fusogen like polyethylene glycol (PEG), the membranes can be merged to re-establish cytoplasmic continuity before degeneration occurs (Ghergherehchi et al., 2019). This intervention allows for the immediate restoration of electrophysiological conduction and significantly improves functional recovery outcomes compared to traditional microsurgical suturing (Riley et al., 2015). Methylene blue and calcium-free solutions are often used as adjuncts to this target to prevent premature membrane sealing and facilitate the fusion process (Bittner et al., 2022).

Other names

Axolemma at transection siteAxonal membraneSevered axonal endsPeripheral nerve stump membranes

Polyethylene glycol (PEG) acts as a molecular fusogen that dehydrates the hydrophilic phospholipid headgroups of the axonal lipid bilayer. This removal of the hydration shell reduces the physical distance and repulsive forces between apposed membranes, allowing the lipid bilayers of the severed proximal and distal axonal ends to merge and restore membrane and cytoplasmic continuity (Bittner et al., 2016; Ghergherehchi et al., 2019).