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Updated: May 27, 2026
Facial Nerve Axotomy in Mice: A Model to Study Motoneuron Response to Injury
Published on: February 23, 2015
Differential activation of proapoptotic molecules between mouse and rat models of distal motor trigeminal denervation
Shiori Harada1, Satoshi O Suzuki, Yoshihiro Seki
1Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Background:
We previously developed a rat trigeminal motor neuron axotomy model involving masseter and temporal muscle resection to study pathological changes of the central nucleus after peripheral nerve injury caused by oral surgery. Because motor neurons are reported to be more vulnerable to axotomy in mice than rats, we compared the degeneration process of the trigeminal motor nucleus in the rat model with a similar mouse model.
Methods:
We removed masseter and temporal muscles of adult mice or rats. Animals were sacrificed at 3, 7, 14, 28, 42, and 56 days post-operation, and the trigeminal motor nuclei were histologically analyzed.
Results:
Size reduction, but no neuronal loss, was seen in the trigeminal motor nuclei in both mice and rats. Time-dependent Noxa expression, starting at 1 week post-operation (wpo), was seen in the mouse model. By 8 wpo, mice expressed a higher level of Noxa than rats. Additionally, we noted persistent expression of cleaved caspase-3 in mice but not in rats. Conversely, apoptosis-inducing factor (AIF), which executes DNA fragmentation in the nucleus, was not translocated to the nucleus in either model.
Conclusions:
Our findings indicate differential activation of motor neuron apoptosis pathways after axotomy in mice and rats. Lack of activation of caspase-independent pathways and distal end denervation in our model might be related to the survival of motor neurons after axonal injury. These findings could be relevant to future neuroprotective strategies for peripheral nerve injury caused by oral surgeries.
Insights
Mice and rats show different motor neuron apoptosis after trigeminal nerve injury. This study compares their responses to aid future neuroprotection strategies for oral surgery nerve damage.
Area of Science:
- Neuroscience
- Cell Biology
- Surgical Research
Background:
- Established a rat model of trigeminal motor neuron axotomy via masseter and temporal muscle resection.
- Investigated pathological changes in the central nucleus post-peripheral nerve injury from oral surgery.
- Compared trigeminal motor nucleus degeneration in mice versus rats due to known differential motor neuron vulnerability.
Purpose of the Study:
- To compare the trigeminal motor nucleus degeneration process in mice and rats following axotomy.
- To elucidate differential apoptotic pathway activation in motor neurons between species after peripheral nerve injury.
Main Methods:
- Adult mice and rats underwent masseter and temporal muscle resection.
- Trigeminal motor nuclei were harvested at multiple time points (3-56 days post-operation).
- Histological analysis was performed to assess neuronal changes and molecular markers.
Main Results:
- Both species exhibited trigeminal motor nucleus size reduction without neuronal loss.
- Mice displayed time-dependent Noxa expression, peaking higher than rats by 8 weeks post-operation.
- Cleaved caspase-3 was persistently expressed in mice but not rats; apoptosis-inducing factor translocation was absent in both.
Conclusions:
- Axotomy triggers differential motor neuron apoptosis pathways in mice and rats.
- The observed motor neuron survival may be linked to the lack of caspase-independent pathway activation and distal denervation.
- Findings offer insights for developing neuroprotective strategies against oral surgery-induced peripheral nerve injuries.
