Synaptic ultrastructure changes in trigeminocervical complex post trigeminal nerve injury

J Comp Neurol, 2016 · DOI: 10.1002/cne.23844 · Published: February 1, 2016

Simple Explanation

Trigeminal nerve injuries can lead to the development of neuropathic pain, which is debilitating and difficult to treat. The goal of the present study was to assess whether there were detectable changes in excitatory or inhibitory synapses in the afferent recipient zone of the trigeminocervical complex in a rat model of chronic constriction injury of the infraorbital nerve (CCI-ION), which leads to orofacial neuropathic pain. Our data indicate that trigeminal nerve injury leads to an increase in R-synaptic profiles (presumably excitatory synapses) and a decrease in R-synaptic length in lamina I of Vc/C2.

Study Duration

3 weeks

Participants

6 adult male Harlan Sprague-Dawley rats

Evidence Level

Not specified

Key Findings

1
Trigeminal nerve injury leads to an increase in R-synaptic profiles (presumably excitatory synapses) in lamina I of Vc/C2.
2
Trigeminal nerve injury leads to a decrease in R-synaptic length in lamina I of Vc/C2.
3
There was a trend for increased F-synapses in lamina II that were not statistically significant by two-way ANOVA with multigroup comparisons, but that did reach statistical significance with uncorrected Fisher’s LSD test.

Research Summary

We examined whether there were changes in the number of different types of synapses during the development of chronic orofacial pain after CCI-ION. Our data indicate that trigeminal nerve injury leads to an increase in R-synaptic profiles (presumably excitatory synapses) and a decrease in R-synaptic length in lamina I of Vc/C2. In conclusion, our findings support that trigeminal nerve injury leads to maladaptive excitatory synaptic plasticity that likely contributes to central sensitization and orofacial neuropathic pain states

Practical Implications

Understanding Neuropathic Pain

The study sheds light on synaptic changes contributing to orofacial neuropathic pain after trigeminal nerve injury.

Targeted Therapies

The findings suggest potential targets for therapeutic interventions aimed at modulating excitatory synapses in the trigeminocervical complex.

Central Sensitization Mechanisms

The research highlights the role of maladaptive excitatory synaptic plasticity in central sensitization processes related to chronic pain.

Study Limitations

1
Low sample size (n=3) may limit the statistical power to detect significant differences.
2
Synapse identification based on ultrastructural morphology may have limitations in distinguishing between R-profiles and C-profiles.
3
The laminar division approach is an estimate only.

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