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Updated: Aug 30, 2026

Facial Nerve Axotomy in Mice: A Model to Study Motoneuron Response to Injury
Published on: February 23, 2015
Natural killer cells do not mediate facial motoneuron survival after facial nerve transection
Susanna C Byram1, Craig J Serpe, Stephen B Pruett
1Department of Cell Biology, Neurobiology and Anatomy, Loyola University Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA. scoers@lumc.edu
Abstract:
The goal of the current study was to determine if natural killer (NK) cells mediate facial motoneuron (FMN) survival following injury. Wild-type (WT), perforin/recombinase activating gene-2 knockout (pfp/RAG-2 KO), and common gamma-chain (gammac)/RAG-2 KO mice received a right facial nerve axotomy. In WT mice, FMN survival was 86+/-1.0% relative to the contralateral control side. In contrast, pfp/RAG-2 and gammac/RAG-2 KO mice exhibited significant decreases in FMN survival ( approximately 20% and approximately 30%, respectively), relative to WT. Reconstitution of pfp/RAG-2 and gammac/RAG-2 KO mice with normal NK cells alone, failed to restore FMN survival levels to those of WT, but did restore functional lytic activity against YAC-1 cells. Reconstitution of pfp/RAG-2 and gammac/RAG-2 KO mice with splenocytes, and pfp/RAG-2 KO mice with CD4+ T-lymphocytes alone or in combination with NK cells, restored FMN survival levels to those of WT. Thus, NK cells appear to not be a component of immune cell-mediated rescue of motoneurons from axotomy induced cell death.
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