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Intra-operative electrical stimulation of non-neuronal cells can improve nerve regeneration across short isografts in a rat model
Grace Catherine Keane, B.A.1, Ellen Larson, B.S.2, Dan A. Hunter, RA3, Deng Pan, BS4, Lauren Schellhardt, BA5, Amy M Moore, MD6, Alison K. Snyder-Warwick, MD7, Matthew Wood, PhD7 and Susan E Mackinnon, MD7, (1)Washington University in Saint Louis School of Medicine, Saint Louis, MO, (2)Washington University in St. Louis, St Louis, MO, (3)Department of Surgery, Division of Plastic and Reconstructive Surgery, Washington University School of Medicine, St Louis, MO, (4)Washington University School of Medicine, St Louis, MO, (5)Washington University School of Medicine, St. Louis, MO, (6)Department of Surgery, Division of Plastic and Reconstructive Surgery, Washington University School of Medicine, Saint Louis, MO, (7)Washington University School of Medicine, Saint Louis, MO

Background: Brief electrical stimulation (BES) of nerves following reconstruction improves axon regeneration and functional recovery in animal models. Presently, studies investigating mechanisms for how BES improves regeneration have focused on a neuron-driven pathway. However, the effects of BES on non-neuronal cells that participate in nerve regeneration remain unstudied. We employed a rat tibial nerve isograft repair model to identify if non-neuronal cells are involved in the effects from BES that improve nerve regeneration.

Methods: Male Lewis rats were randomized to four groups: Graft-Donor EStim, Nerve-Recipient EStim, EStim (positive control) and Control (negative control). The three groups utilizing BES were stimulated during surgery for 1 hour at 16 Hz and 0.5 mA. For the Graft-Donor EStim group, the nerve was cut and stimulated distal to the cut, then the nerve was used as a 1 cm isograft to repair a tibial nerve injury in a recipient rat. In the Nerve-Recipient EStim group, the tibial nerve of a recipient rat was transected and stimulated proximal to the injury site, then an unstimulated 1 cm isograft was used to repair the nerve. For the EStim and Control groups, tibial nerve was transected and repaired with a 1 cm isograft, where the EStim group received BES after repair. Isografts and distal nerve were harvested at either 1 or 2 week endpoints for immunohistochemical analysis of axonal regeneration (b-III-Tubulin density) or cellular populations, or evaluated using qRT-PCR for select genes.

Results: There was an increase in b-III-Tubulin density inthe three BES groups compared to the Control group at all points along the isograft (p<.001). As well, therewas no significant difference in the means of b-III-Tubulin density of Graft-Donor EStim, Nerve-Recipient EStim, or EStim groups at the mid-graft (p=.23), distal-graft (p=.63) or distal nerve end (p=.28). Further evaluation of the Graft-Donor EStim group revealed that BES to the graft alone resulted in increased macrophage accumulation and macrophage recruiting gene expression.

Conclusions: BES had an impact on non-neuronal cells, where these results suggest that BES promotes changes to non-neuronal cells that in turn promote nerve regeneration.


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