Polyethylene glycol restores axonal conduction after corpus callosum transection

Polyethylene glycol（PEG） has been shown to restore axonal continuity after peripheral nerve transection in animal models. We hypothesized that PEG can also restore axonal continuity in the central nervous system. In this current experiment, coronal sectioning of the brains of Sprague-Dawley rats was performed after animal sacrifice. 3Brain high-resolution microelectrode arrays（MEA） were used to measure mean firing rate（MFR） and peak amplitude across the corpus callosum of the ex-vivo brain slices. The corpus callosum was subsequently transected and repeated measurements were performed. The cut ends of the corpus callosum were still apposite at this time. A PEG solution was applied to the injury site and repeated measurements were performed. MEA measurements showed that PEG was capable of restoring electrophysiology signaling after transection of central nerves. Before injury, the average MFRs at the ipsilateral, midline, and contralateral corpus callosum were 0.76, 0.66, and 0.65 spikes/second, respectively, and the average peak amplitudes were 69.79, 58.68, and 49.60 μV, respectively. After injury, the average MFRs were 0.71, 0.14, and 0.25 spikes/second, respectively and peak amplitudes were 52.11, 8.98, and 16.09 μV, respectively. After application of PEG, there were spikes in MFR and peak amplitude at the injury site and contralaterally. The average MFRs were 0.75, 0.55, and 0.47 spikes/second at the ipsilateral, midline, and contralateral corpus callosum, respectively and peak amplitudes were 59.44, 45.33, 40.02 μV, respectively. There were statistically differences in the average MFRs and peak amplitudes between the midline and non-midline corpus callosum groups（P 〈 0.01, P 〈 0.05）. These findings suggest that PEG restores axonal conduction between severed central nerves, potentially representing axonal fusion.

A novel technique using hydrophilic polymers to promote axonal fusion

The management of traumatic peripheral nerve injury remains a considerable concern for clinicians.With minimal innovations in surgical technique and a limited number of specialists trained to treat peripheral nerve injury,outcomes of surgical intervention have been unpredictable.The inability to manipulate the pathophysiology of nerve injury（i.e.,Wallerian degeneration） has left scientists and clinicians depending on the slow and lengthy process of axonal regeneration（-1 mm/day）.When axons are severed,the endings undergo calcium-mediated plasmalemmal sealing,which limits the ability of the axon to be primarily repaired.Polythethylene glycol（PEG） in combination with a bioengineered process overcomes the inability to fuse axons.The mechanism for PEG axonal fusion is not clearly understood,but multiple studies have shown that a providing a calcium-free environment is essential to the process known as PEG fusion.The proposed mechanism is PEG-induced lipid bilayer fusion by removing the hydration barrier surrounding the axolemma and reducing the activation energy required for membrane fusion to occur.This review highlights PEG fusion,its past and current studies,and future directions in PEG fusion.