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Updated: Apr 10, 2026
Facial Nerve Axotomy in Mice: A Model to Study Motoneuron Response to Injury
Published on: February 23, 2015
Layer 5 Pyramidal Neurons' Dendritic Remodeling and Increased Microglial Density in Primary Motor Cortex in a Murine
Diana Urrego1, Julieta Troncoso2, Alejandro Múnera3
1Behavioral Neurophysiology Laboratory, Universidad Nacional de Colombia, 111321 Bogotá, Colombia ; Department of Molecular Biology of Neuronal Signals, Max-Planck Institute for Experimental Medicine, 37075 Goettingen, Germany.
Abstract:
This work was aimed at characterizing structural changes in primary motor cortex layer 5 pyramidal neurons and their relationship with microglial density induced by facial nerve lesion using a murine facial paralysis model. Adult transgenic mice, expressing green fluorescent protein in microglia and yellow fluorescent protein in projecting neurons, were submitted to either unilateral section of the facial nerve or sham surgery. Injured animals were sacrificed either 1 or 3 weeks after surgery. Two-photon excitation microscopy was then used for evaluating both layer 5 pyramidal neurons and microglia in vibrissal primary motor cortex (vM1). It was found that facial nerve lesion induced long-lasting changes in the dendritic morphology of vM1 layer 5 pyramidal neurons and in their surrounding microglia. Dendritic arborization of the pyramidal cells underwent overall shrinkage. Apical dendrites suffered transient shortening while basal dendrites displayed sustained shortening. Moreover, dendrites suffered transient spine pruning. Significantly higher microglial cell density was found surrounding vM1 layer 5 pyramidal neurons after facial nerve lesion with morphological bias towards the activated phenotype. These results suggest that facial nerve lesions elicit active dendrite remodeling due to pyramidal neuron and microglia interaction, which could be the pathophysiological underpinning of some neuropathic motor sequelae in humans.
Insights
Facial nerve injury causes lasting changes in motor cortex neurons and increased activated microglia. This neuron-microglia interaction may underlie motor deficits after nerve damage.
Area of Science:
- Neuroscience
- Cell Biology
- Motor System Research
Background:
- Facial nerve lesions can lead to motor impairments.
- Understanding neuronal and glial responses is crucial for developing treatments.
Purpose of the Study:
- To investigate structural changes in primary motor cortex layer 5 pyramidal neurons.
- To examine the relationship between these neuronal changes and microglial density after facial nerve injury.
Main Methods:
- Utilized a murine model of facial paralysis.
- Employed two-photon excitation microscopy to analyze neuronal morphology and microglial density in the vibrissal primary motor cortex (vM1).
- Assessed changes at 1 and 3 weeks post-lesion.
Main Results:
- Facial nerve lesions induced significant, long-lasting alterations in vM1 layer 5 pyramidal neuron dendritic morphology, including shrinkage and spine pruning.
- A notable increase in microglial density and a shift towards an activated phenotype were observed around these neurons.
- Apical dendrites showed transient shortening, while basal dendrites exhibited sustained shortening.
Conclusions:
- Facial nerve lesions trigger active dendritic remodeling in pyramidal neurons.
- The interaction between neurons and microglia plays a key role in these structural changes.
- This remodeling may represent a pathological mechanism contributing to human neuropathic motor sequelae.
