Flow cytometry analysis of immune and glial cells in a trigeminal neuralgia rat model

Abstract

Microvascular compression of the trigeminal root entry zone (TREZ) is the main cause of most primary trigeminal neuralgia (TN), change of glial plasticity was previously studied in the TREZ of TN rat model induced by chronic compression. To better understand the role of astrocytes and immune cells in the TREZ, different cell markers including glial fibrillary acidic protein (GFAP), complement C3, S100A10, CD45, CD11b, glutamate-aspartate transporter (GLAST), Iba-1 and TMEM119 were used in the TN rat model by immunohistochemistry and flow cytometry. On the post operation day 28, GFAP/C3-positive A1 astrocytes and GFAP/S100A10-positive A2 astrocytes were activated in the TREZ after compression injury, there were no statistical differences in the ratios of A1/A2 astrocytes between the sham and TN groups. There was no significant difference in Iba-1-positive cells between the two groups. The ratios of infiltrating lymphocytes (CD45+CD11b−) (p = 0.0075) and infiltrating macrophages (CD45highCD11b+) (p = 0.0388) were significantly higher than those of the sham group. In conclusion, different subtypes A1/A2 astrocytes in the TREZ were activated after compression injury, infiltrating macrophages and lymphocytes increased, these neuroimmune cells in the TREZ may participate in the pathogenesis of TN rat model.

A comprehensive two-sample Mendelian randomization analysis of trigeminal neuralgia and modifiable risk factors

“…Infiltrating macrophages and lymphocytes were found to be increased in the trigeminal neuralgia rat model. This suggests that neuroimmune cells may be involved in the pathogenesis of the TN rat model (42). Of course the mechanisms need to be further studied.…”

Preclinical orofacial pain assays and measures and chronic primary orofacial pain research: where we are and where we need to go

“…Both CCT and sham-operated animals develop heat-hypersensitivity over the course of 4 weeks ( 201 ). Activation and increase in the numbers of Schwann cells, astrocytes (i.e., A1-astrocytes) and microglia/macrophages, as well as an increase in the infiltration of macrophages and lymphocytes in the trigeminal root zone are also seen 4 weeks following CCT, suggesting the contributions of neuroimmune cells to the pathogenesis of TN attributed to neurovascular compression ( 203 , 221 ).…”

Compression Degree of Trigeminal Nerve and Type of Conflicting Vessels Determine Short- and Long-Term Complete Pain Relief in Adult Patients with Primary Trigeminal Neuralgia After Microvascular Decompression: A Three-Year Retrospective Study of 200 Adult Patients with Primary Trigeminal Neuralgia

“…4 In addition to other unknown etiologies, pathological demyelination along the trigeminal afferent pathway triggered by neurovascular conflict (NVC) with physical compression and morphological changes of TN is the predominant pathogenesis and pathophysiological mechanism of PTN, and subsequent activated neuroimmune cells, released inflammatory cytokines, significant molecular changes, channelopathies, and electrophysiological abnormalities pave the way for a generation of ectopic impulses and ephaptic crosstalk. 1,[5][6][7][8][9] In adult patients with PTN, three-dimensional time-of-flight magnetic resonance angiography (3D-TOF-MRA) prior to surgery has demonstrated a better capacity to identify the presence of NVC with nearby specific offending vessels, and thus neuroimaging using magnetic resonance imaging (MRI) with high resolution can be available as a reliable objective imaging predictor of therapeutic responsiveness and outcome to neurosurgical interventions. 10,11 The initial standard management of adult patients with PTN is conventional pharmacotherapy with different action mechanisms, either monotherapy or combination therapy.…”