EXPERIMENTAL TRIGEMINAL NEURALGIA OF INFRAORBITAL NERVE CAUSES MORPHOLOGICAL PERIPHERICAL CHANGES
Authors: da Silveira Helson Freitas , Alves Luíza Clertiani Vieira , Gondim Delane Viana , de Oliveira Sousa Kalina Kelma , Dias Diego Bernarde Souza , Vale Mariana Lima 
Published: June 2021

The Trigeminal Neuralgia (TN) is a chronic disease and the most common and severe neuropathy in head and neck, that causes suffering and decrease the life quality of pacients and almost always it conducts to alodinia. It is characterized by shoots of pain in the trigeminal nerve region. It is believed that the trigeminal pain etiology is related of lesions in trigeminal nerve branches as demyelization. Neuronal injury conduct to neuroplasticity changes fallowed by central and peripheral sensitization, In addition, it is still unclear how morphological changes in the trigeminal pathway behave after a neuronal injury and its relationship with nociceptive response. The aim of this study was to evaluate the peripheral morphological changes in the trigeminal pathway in model of neuralgia of infraorbital nerve in rats. Eighteen male Wistar rats (180–220 g), originating from the Central Animal Facility of the Federal University of Ceará ‐ Brazil, kept at 22 °C, by day/night cycle ‐ 12/12 h, with water and food ad libitum were used. The rats were divided into 3 groups: control (C), Trigeminal Neuralgia (TN) and TN Sham. The TN was induced by infraorbital nerve (ION) constriction model, through a loose ligature on the rostral portion of the nerve. It was performed the measurement of nociceptive threshold using an electronic an algesimeter (Von Frey) twice per week, on days 0, 3, 7, 10, 14, 18 and 21 after TN surgery. The animals were euthanized and the ION, and vibrissal skin were collected. Immunofluorescence analysis was performed using the anti‐MBP and DAPI antibody in nerve and anti‐PGP9.5 and DAPI in vibrissal skin. Images of immunofluorescence were capture in a confocal microscopy and quantified the intensity of marking using the ImageJ software. Statistical analysis was performed by mean ± SEM of the measures recorded, by Student t test or ANOVA analyze, followed by Tukey or Games Howell pos‐hoc test, based on Levene's homogeneity teste, both with significance level p<0.05 using SPSS 20.0 software. In the analysis of the nociceptive threshold for 21 days post‐induction (Figure 1A), it was verified that the TN group showed a very reduced nociceptive threshold in relation to Control and TN Sham groups (p<0.0001) and no significance between Control and TN Sham groups (p=0.989), that confirms the presence of neuropathic pain. When we analyzed the anti‐MBP markers on ION, a significant increase in MPB expression was identified in the TN group (p<0.0001) indicating a significant axonal lesion with a response of nerve through a MPB production (Figure 2A and 2C). In addition, we observed through DAPI marker on ION, that there is a probable large migration of macrophages the nerve (FIGURE 2B and 2C), that is essential to signalization to MBP Schwann cells production. As a consequence of this alterations, we found too, a reduction number of nervous endings in vibrissal skin, shown by the marker PGP9.5 expression (p<0.0001) (FIGURE 1B and 1C). Thus, we conclude that the trigeminal neuralgia caused by peripheral injury conduct a loss of nervous terminations with a reaction of nerve to a possible repair, that could be a cause of a peripheral sensitization, reducing the nociceptive threshold. Thus, we hypothesize that a possible failure in remyelination, axonal loss and degeneration of the fibers and nerve endings, leading to nerve conduction failure of the nociceptive signals, leading to hypersensitivity.

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.