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Herpes simplex keratitis(HSK), caused by the infection of herpes simplex virus type Ⅰ(HSV-1)in cornea, is a global blinding corneal disease. After the primary infection in ocular surface, HSV-1 is transported into trigeminal ganglion and establishes the life-lasting latency, and it results in recurrent keratopathy. In the process of studying the latent mechanism of HSV, it has been gradually recognized that both the virus itself and the host response regulate the latent process of HSV. In recent years, a large number of research results have been obtained on the molecular mechanisms of invasion, immunity, latency and recurrence of neurotropic viruses, which provide new ideas for the prevention and treatment of HSK. In the present review, the recent progress of HSV latency mechanism in trigeminal ganglion after the primary infection in corneal surface was introduced, and the unsolved basic and clinical problems in HSK were discussed.
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Migraine is a common and debilitating headache disorder. Although its pathogenesis remains elusive, abnormal trigeminal and central nervous system activity is likely to play an important role. Transient receptor potential (TRP) channels, which transduce noxious stimuli into pain signals, are expressed in trigeminal ganglion neurons and brain regions closely associated with the pathophysiology of migraine. In the trigeminal ganglion, TRP channels co-localize with calcitonin gene-related peptide, a neuropeptide crucially implicated in migraine pathophysiology. Many preclinical and clinical data support the roles of TRP channels in migraine. In particular, activation of TRP cation channel V1 has been shown to regulate calcitonin gene-related peptide release from trigeminal nerves. Intriguingly, several effective anti-migraine therapies, including botulinum neurotoxin type A, affect the functions of TRP cation channels. Here, we discuss currently available data regarding the roles of major TRP cation channels in the pathophysiology of migraine and the therapeutic applicability thereof.
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Trigeminal neuropathic pain (TNP) is a significant health problem but the involved mechanism has not been completely elucidated. Toll-like receptors (TLRs) have recently been demonstrated to be expressed in the dorsal root ganglion and involved in chronic pain. Here, we show that TLR8 was persistently increased in the trigeminal ganglion (TG) neurons in model of TNP induced by partial infraorbital nerve ligation (pIONL). In addition, deletion or knockdown of Tlr8 in the TG attenuated pIONL-induced mechanical allodynia, reduced the activation of ERK and p38-MAPK, and decreased the expression of pro-inflammatory cytokines in the TG. Furthermore, intra-TG injection of the TLR8 agonist VTX-2337 induced pain hypersensitivity. VTX-2337 also increased the intracellular Ca
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OBJECTIVE@#To observe the effect of occlusal interference on the afferent pathway of the trigeminal nerve and neuronal excitability in the trigeminal subnucleus caudalis (SPVC) of rats by electrical stimulation of the trigeminal ganglion (TG) and extracellular recordings of SPVC activities.@*METHODS@#Twenty male Wistar rats were randomly divided into control group and model group (=10). In the model group, occlusal interference for 30 consecutive days was induced using light-cured flowable resin on the right maxillary molars. During occlusal interference, the pain sensitivity was scored with von Frey Fibers in the masseter. Simultaneous recordings of electrical activities from the SPVC, electrocardiogram, body temperature and electromyogram of the breath muscles of the anesthetized rats were performed, and the responses evoked by electrical stimulation of the TG were analyzed.@*RESULTS@#Compared with the control rats, the rats in the model group showed significantly increased pain sensitivity scores ( 0.05). Train stimulation (0.2 ms, 1 mA, 30 s, 100 Hz) of the TG significantly increased the discharge frequency of the SPVC only in the rats in the model group ( < 0.05).@*CONCLUSIONS@#The functional activities of the pain afferent pathway of the trigeminal nerve can be electrophysiologically monitored by electrical stimulation of the TG and extracellular recordings of SPVC activities in rats. Occlusal interference can increase the excitability of the neurons in the SPVC and enhance their sensitivities to TG afferent activation, suggesting the neural plasticity of the pain afferent pathway.
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It is well known that trigeminal nerve injury causes hyperexcitability in trigeminal ganglion neurons, which become sensitized. Long after trigeminal nerve damage, trigeminal spinal subnucleus caudalis and upper cervical spinal cord (C1/C2) nociceptive neurons become hyperactive and are sensitized, resulting in persistent orofacial pain. Communication between neurons and non-neuronal cells is believed to be involved in these mechanisms. In this article, the authors highlight several lines of evidence that neuron-glial cell and neuron macrophage communication have essential roles in persistent orofacial pain mechanisms associated with trigeminal nerve injury and/or orofacial inflammation.
Subject(s)
Cell Communication , Cervical Cord , Facial Pain , Inflammation , Macrophages , Neurons , Nociceptors , Trigeminal Ganglion , Trigeminal Nerve , Trigeminal Nerve Injuries , Trigeminal Nucleus, SpinalABSTRACT
Aim: To observe the expression changes of brain-derived neurotropic factor (BDNF) and receptor TrkB in trigeminal ganglion (TG) of trigeminal neuralgia (TN) rats. Methods: Animal model of TN was established using the infraorbital nerve chronic injury compression model (ION-CCI). The sham operation group (sham group) and the TN model group were composed of randomly divided 180 - 220 g SD male rats. The mechanical threshold of the injury side of the two groups was determined. Quantitative real-time PCR (qPCR), immunohistochemistry and immunfluorescence methods were used to detect the expression of BDNF, TrkB, pro-inflammatory TNF-α and IL-1B in the injured TGs. Results: After two weeks of modeling, the mechanical pain threshold was significantly down-regulated in TN group compared to sham group (P<0. 05). The expression of BDNF and TrkB in TGs of TN group was significantly higher than that in sham operation group. Besides, the levels of pro-inflammatory factors TNF-a and IL-1β also significantly increased in TGs of TN group compared with sham group (P < 0. 05). Conclusions: The expression of BDNF and TrkB in TG of ION-CCI rats increases in trigeminal neuralgia group, which may be involved in the pathogenesis of trigeminal neuralgia and promote the pain transmission of trigeminal neuralgia.
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Aquaporin 1 (AQP1) is an aquaporin distributed in the peripheral nervous system. It has been found in neurons and glial cells of peripheral nerve structures, including trigeminal ganglion, dorsal root ganglion and enteric nervous system. AQP1 may be involved in the regulation of water balance of ganglia and nerve fiber bundles in the peripheral nervous system under physiological and pathological conditions, and plays a key role in maintaining the intracellular and extracellular water balance of peripheral nervous system under pathological condition. Knowing the structure and function of AQP1 can contribute to the understanding of the pathophysiology of the nervous system, providing new ways and methods for clinical treatment. This review summarizes the recent researches on AQP1.
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Objective To investigate the effect of the interaction between satellite glial cells and neurons in the trigeminal ganglion of trigeminal neuralgia (TN) rat model. Methods In the TN rat model (n = 24) induced by trigeminal root entry zone chronic compression and sham group (n = 24), immunofluorescence and Western blotting were used to detect the expression of myelin basic protein (MBP), glial fibrillary acidic protein (GFAP) and of P75 neurotrophic factor receptor (P75) in the trigeminal ganglion. Results The expression of P75NTR in TN group was higher than that in the sham operation group, especially on the post-operation day (POD) 7 and 14 (P<0.01). The expression of MBP in the TN group was decreased after operation, which were significant lower than that in the sham operation group on POD 7 and 14 (P<0.05). While the expression of immunoreactive GFAP in the satellite glial cells in the TN group was higher than that in the sham operation group from POD 7 to POD 21 after operation (P<0.01). Conclusion The changes of MBP and P75NTR expression in neurons and the activation of satellite glial cells in trigeminal ganglion of the TN animal model may affect the interaction of neuron-satellite glial cells, which may be involved in the nociceptive information transmission from orofacial area to the central nervous system in the TN rats.
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Objective To compare the efficacy of adriamycin chemo-ganglionectomy and radiofre-quency thermocoagulation ( RFT ) of semilunar ganglion in treating craniofacial postherpetic neuralgia ( PHN) . Methods A total of 95 patients with PHN in the areas innervated by maxillary and mandibular divisions of trigeminal nerve, aged 55-90 yr, with the course of disease 6 months-3 yr, were divided into 2 groups using a random number table method: adriamycin chemo-ganglionectomy group ( ADM group, n=48) and RFT group ( n=47) . Hartel anterior approach to puncture was performed via the foramen ovale un-der the guidance of CT in two groups. In group ADM, 0. 5％ adriamycin 2. 5 mg ( 0. 5 ml) was injected via the foramen ovale, and RFT of gasserian ganglion was performed in group RFT. Visual Analog Scale (VAS) and the short-form McGill pain questionnaire (SF-MPQ) scores were evaluated before and after treatment. The rate of effective treatment was calculated, and treatment-related complications were recor-ded. Results Compared with group RFT, no significant change was found in VAS or SF-MPQ scores be-fore treatment, VAS and SF-MPQ scores were increased and the rate of effective treatment was decreased at 1 and 7 days after treatment, VAS and SF-MPQ scores were decreased and the rate of effective treatment was increased at 6 and 12 months after treatment, the incidence of facial numbness, hypoesthesia, masti-catory muscle weakness and weakened corneal reflex was decreased in group ADM ( P<0. 05) . Conclusion Compared with semilunar ganglion RFT, the long-term efficacy of adriamycin chemo-ganglionectomy of semilunar ganglion in treating craniofacial PHN is enhanced, and the safety is higher.
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The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome is the most frequently studied in the central nervous system and has been linked to neuropathic pain. In this study, a post-translational mechanism of microRNA (miR)-186 via regulating the expression of NLRP3 in the complete Freund's adjuvant (CFA)-treated mice was investigated. The injection of CFA was used to induce trigeminal neuropathic pain in mice. miRs microarray chip assay was performed in trigeminal ganglions (TGs). CFA treatment significantly increased the mRNA expression of NLRP3, interleukin (IL)-1β, and IL-18 in TGs compared to the control group. Moreover, 26 miRs were differentially expressed in TGs from trigeminal neuropathic pain mice, and the expression of miR-186 showed the lowest level of all the miRs. Further examination revealed that NLRP3 was a candidate target gene of miR-186. We delivered miR-186 mimics to CFA-treated mice. The head withdrawal thresholds of the CFA-treated mice were significantly increased by miR-186 mimics injection compared with CFA single treatment. The mRNA and protein expression of NLRP3, IL-1β, and IL-18 in TGs from trigeminal neuropathic pain mice were significantly inhibited by miR-186 mimics treatment compared to the CFA group. miR-186 was able to suppress the neuropathic pain via regulating the NLRP3 inflammasome signaling.
Subject(s)
Animals , Male , Trigeminal Neuralgia/drug therapy , MicroRNAs/pharmacology , Inflammasomes/physiology , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Reference Values , Time Factors , Enzyme-Linked Immunosorbent Assay , Random Allocation , Freund's Adjuvant , Blotting, Western , Interleukin-18/analysis , Interleukin-18/metabolism , Microarray Analysis , Disease Models, Animal , Interleukin-1beta/analysis , Interleukin-1beta/metabolism , Genetic Association Studies , Inflammasomes/analysis , NLR Family, Pyrin Domain-Containing 3 Protein/analysis , Luciferases , Mice, Inbred C57BLABSTRACT
In this work, we established an in vivo murine model of herpes simplex virus type 1 (HSV1) infection involving inoculation by scarification of the oral mucosain order to study its dissemination towards the trigeminal ganglion (TG). Both viral DNA and infectious virions were detected on the third day postinfection (p.i.). Viral proteins revealed by immunohistochemistry were mainly found at seven days p.i., when the latencyassociated transcript (LAT) was also detected. This model simulated the dissemination process of HSV1, which could be used to study herpes pathogenesis starting in the oral mucosa (AU)
Con el propósito de estudiar la dispersión de del Herpes Simplex Virus tipo 1 (HSV1) desde la mucosa oral hasta los ganglios trigeminales, en el presente trabajo se estableció un modelo de infección en ratones, haciendo inoculación por escarificación en la mucosa oral. Tanto ADN viral como viriones infecciosos se detectaron en los ganglios trigeminales al dia 3 postinfección (p.i.). Las proteínas virales se detectaron principalmente al día 7 p.i. cuando los transcritos asociados a latencia también fueron encontrados. El modelo de infección simula adecuadamente el proceso de dispersión del HSV1 y puede ser usado para el estudio de la patogénesis por herpes después de la infección primaria en la mucosa oral (AU)
Subject(s)
Animals , Mice , Herpesvirus 1, Human , Mouth Mucosa , Trigeminal Ganglion , Colombia , DNA, Viral , Virus LatencyABSTRACT
ABSTRACT Objectives The aim of this study was to explore the effect of capsaicin on expression patterns of calcitonin gene-related peptide (CGRP) in the trigeminal ganglion (TG) and trigeminal subnucleus caudalis (Vc) following experimental tooth movement. Material and Methods Male Sprague-Dawley rats were used in this study and divided into small-dose capsaicin+force group, large-dose capsaicin+force group, saline+force group, and no force group. Closed coil springs were used to mimic orthodontic forces in all groups except for the no force group, in which springs were inactivated. Capsaicin and saline were injected into periodontal tissues. Rats were euthanized at 0 h, 12 h, 1 d, 3 d, 5 d, and 7 d following experimental tooth movement. Then, TG and Vc were obtained for immunohistochemical staining and western blotting against CGRP. Results Immunohistochemical results indicated that CGRP positive neurons were located in the TG, and CGRP immunoreactive fibers were distributed in the Vc. Immunohistochemical semiquantitative analysis and western blotting analysis demonstrated that CGRP expression levels both in TG and Vc were elevated at 12 h, 1 d, 3 d, 5 d, and 7 d in the saline + force group. However, both small-dose and large-dose capsaicin could decrease CGRP expression in TG and Vc at 1 d and 3 d following experimental tooth movement, as compared with the saline + force group. Conclusions These results suggest that capsaicin could regulate CGRP expression in TG and Vc following experimental tooth movement in rats.
Subject(s)
Animals , Male , Tooth Movement Techniques/methods , Trigeminal Caudal Nucleus/drug effects , Capsaicin/pharmacology , Calcitonin Gene-Related Peptide/drug effects , Trigeminal Ganglion/drug effects , Sensory System Agents/pharmacology , Reference Values , Time Factors , Trigeminal Caudal Nucleus/chemistry , Facial Pain , Immunohistochemistry , Sodium Chloride , Random Allocation , Calcitonin Gene-Related Peptide/analysis , Blotting, Western , Trigeminal Ganglion/chemistry , Reproducibility of Results , Rats, Sprague-DawleyABSTRACT
Our previous study found that some trigeminal ganglion (TG) nerve endings in the inner walls of rat anterior chambers were mechanosensitive, and transient receptor potential ankyrin 1 (TRPA1) was an essential mechanosensitive channel in the membrane. To address the effect of cannabinoids on the mechanosensitive TG nerve endings in the inner walls of anterior chambers of rat eye, we investigated the effect of the (R)-(+)-WIN55, 212-2 mesylate salt (WIN), a synthetic cannabinoid on their cell bodies in vitro. Rat TG neurons innervating the inner walls of the anterior chambers were labeled by 1,1'-dilinoleyl-3,3,3',3'-tetramethylindocarbocyanine, 4-chlorobenzenesulfona (FAST DiI). Whole cell patch clamp was performed to record the currents induced by drugs and mechanical stimulation. Mechanical stimulation was applied to the neurons by buffer ejection. WIN evoked inward currents via TRPA1 activation in FAST DiI-labeled TG neurons. WIN enhanced mechanosensitive currents via TRPA1 activation in FAST DiI-labeled TG neurons. Our results indicate that cannabinoids can enhance the mechanosensitivity of TG endings in the inner walls of anterior chambers of rat eye via TRPA1 activation.
Subject(s)
Animals , Rats , Action Potentials , Anterior Chamber , Cannabinoids , Eye , Neurons , Patch-Clamp Techniques , Rats, Sprague-Dawley , TRPA1 Cation Channel , TRPC Cation Channels , Genetics , Trigeminal Ganglion , PhysiologyABSTRACT
Objective: To characterize a neuron-enriched primary TG culture and evaluate interferon- β expression and activity after HSV-1 infection. Materials and methods: The percentage of neurons present in cultures was assessed by neurofilament immunocytochemistry. Cultures were treated with interferon- β and infected with HSV-1, then viral antigen positive cells were counted and interferon- βexpression was assessed by quantitative PCR. Results: The culture contained 15% neurons and 85% non-neuronal cells. A cytopathic effect was observed, associated with high viral spread (72.9% neurons and 48.3% non-neuronal cells were positive for viral antigen). Interferon- β treatment impaired the cytopathic effect and decreased the infected neurons to 16.7% and infected non-neuronal cells to 7.8%. Viral infection at 6 h postinfection significantly increased the interferon- β transcripts by 18.2 fold, while at 18 h postinfection Interferon pre-treatment in infected cultures increased interferon- β transcription by 3.7 fold. Discussion: This culture model contained 15% neurons, which is 10 times higher compared to other reported cultures, and non-neuronal cells comprised 85% of cells in this culture. All types of cells were found to be infected, which is similar to that reported during acute infections in vivo . Additionally, interferon- βdecreased the infected cells, avoiding the cytopathic effect, which is similar to that reported in swine TG cultures. Conclusions: A neuron-enriched primary TG model was characterized. Interferon- β treatment protected cells from cytopathic effects and viral spread, while viral infection up-regulated interferon- β expression. This result means that interferon- β exerts an important antiviral effect against HSV-1 in these cultures.
Objetivo: Caracterizar un cultivo primario de ganglio trigeminal (GT) enriquecido en neuronas y evaluar la expresión de interferón- y su actividad frente a la infección con Herpes simple tipo 1 (HSV-1). Materiales y métodos: El porcentaje de neuronas fue determinado por inmunocitoquímica para neurofilamento. Los cultivos fueron tratados con interferón- β e infectados con HSV-1, y se cuantificaron las células positivas para antígeno viral por inmunocitoquímica y la expresión de interferón- β por PCR cuantitativa. Resultados: El cultivo presentó un 15% de neuronas y 85% de células no neuronales. Se encontró efecto citopático, asociado a una alta diseminación de la infección (72,9% neuronas y 48,3% de células no neuronales positivas para antígeno viral). El interferón- β evitó la aparición de efecto citopático y disminuyó las células infectadas a 16,7% en neuronas y a 7,8% las células no neuronales. La infección viral incrementó la expresión de transcritos de interferón- β 18,2 veces a las 6 h de infección, mientras que a las 18 h post infección el tratamiento con interferón incrementó esta expresión 3,7 veces. Discusión: Los cultivos presentaron un 15% de neuronas, lo cual es 10 veces más que en otros cultivos reportados. Las células no neuronales representan el 85% de las células del cultivo, y se evidenció que todos los tipos de células se infectaron; similar a lo que ha sido reportado durante infecciones agudas in vivo . Adicionalmente, el interferón- β disminuyó el porcentaje de células infectadas y evitó la aparición de efecto citopático, similar a lo que ha sido reportado en cultivos de GT porcino. Conclusiones: Se caracterizó un modelo de cultivo primario de GT enriquecido en neuronas. Interferón- β protegió las células del efecto citopático y la diseminación viral mientras que la infección viral incrementó la expresión de interferón- β. Por lo tanto, el interferón- β ejerció un papel antiviral importante frente al HSV-1 en estos cultivos.
Subject(s)
Humans , Animals , Mice , Trigeminal Ganglion , Herpesvirus 1, Human , Neurons , Intermediate Filaments , Interferons , Ganglia, Sensory , InfectionsABSTRACT
Objective To observe the efficacy of Mimics finite element analysis software in the gasserian ganglion radiofrequency treatment of trigeminal neuralgia. Methods 180 cases with primary trigeminal neuralgia and VAS score ≥8 were randomly divided into 2 groups (n = 90 each): CT group (group C) and Mimics group (group M). The preoperative skull CT image of the foramen of cranial base could be analyzed in group C. The preoperative cranial CT image could be reconstructed and analyzed by Mimics finite element analysis software in group M. The puncturing success rate, complications rate and the outcomes between two groups were recorded. Results The puncturing success rates were 100% in group M and 92% in group C (P 0.05) between them. Conclusions The Mimics finite element analysis software could improve the success rate of basicranial foramen ovale puncture and reduce the occurrence rate of puncture complications. Therefore , it could be safely applied to the treatment of primary trigeminal neuralgia by gasserian ganglion radio frequency.
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Objective This study assesses the influence of rizatriptan on calcitonin gene-related peptide (CGRP),proenkephalin (PENK) and cholecystokinin (CCK) mRNA expressions in the trigeminal ganglia of a rat migraine model and investigates the possible mechanisms by which triptans treat migraine.Methods A total of 24 rats were randomly divided into four groups:normal control group (A),migraine model group(B),rizatriptan control group (C) and rizatriptan treatment group(D).Groups C and D were intragastrically perfused with rizatriptan,1 mg/kg per day.After 7 days,nitroglycerin was subcutaneously injected into the buttocks of the groups B and D to induce migraine.Two hours after nitroglycerin injection,the trigeminal ganglia was isolated.CGRP,PENK and CCK mRNA expressions in the trigeminal ganglia were determined using SYBR Green Ⅰ real-time quantitative PCR.Results The copy number of CGRP mRNA (× 107) in 200 ng total RNA of each group was 0.05 ±0.01,1.30 ±0.52,0.23 ±0.12,0.43 ±0.33 ; The copy number of PENK mRNA (× 103) in 200 ng total RNA of each group was 3.30 ± 1.65,0.34 ±0.14,3.91 ± 2.44,0.71 ± 0.13.The copy number of CGRP mRNA in the trigeminal ganglia of group B was significantly higher than that of group A (q =7.854,P ＜ 0.05) ; CGRP mRNA expressions were significantly lower in the trigeminal ganglia of rats in group D compared with group B (q =5.458,P ＜0.05).Compared with group A,PENK mRNA expressions in the trigeminal ganglia of rats were significantly lower in group B (q =4.478,P ＜ 0.05).PENK mRNA expressions were significantly higher in trigeminal ganglia of rats in group C compared with group D (q =4.838,P ＜ 0.05).CCK mRNA expression in trigeminal ganglia of rats was similar among groups.Conelusions Rizatriptan can decrease the expressions of CGRP in the trigeminal ganglia of the migraine rats and exhibits neurogenic inflammation triggered by CGRP.PENK expressions decrease in the trigeminal ganglia of the migraine rats,weaken the analgesic effects of enkephalin.
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BACKGROUND: To evaluate the results of conventional radiofrequency thermorhizotomy (CRT) for trigeminal neuralgia (TN) in patients with failed medical management. METHODS: Patients with Trigeminal neuralgia who were referred to us for 'limited intervention' during the time frame July-2011 to Jan-2013 were enrolled for this study. CRT was administered by the Sweet technique. Pain relief was evaluated by the principle investigator. RESULTS: Eighteen patients were enrolled and completed a mean follow-up of 18.0 months. Pain relief was observed in 14 of 18 (77.8%) patients on the post-operative day, 14 of 18 (77.8%) at 1-month follow-up, 14 of 17 (82.4%) at 3-months follow-up, 12 of 15 (80%) at 6-months follow-up, 7 of 11 (63.6%) at 1-year follow-up and 2 of 6 (33.3%) 1.5 years of follow-up. Four patients required a repeat cycle of CRT; two at six months of follow-up and two at one year of follow-up. One patient was transferred for surgical intervention at six months of follow-up. Side-effects included facial hypoesthesia (n = 6); nausea/vomiting (n = 2), diminished corneal reflex (n = 13) and difficulty in chewing (n = 11). Severity of adverse effects gradually diminished and none of the patients who are beyond 6 months of follow-up have any functional limitation. CONCLUSIONS: CRT is an effective method of pain relief for patients with Trigeminal neuralgia. Successful outcome (excellent or good) can be expected in 66.7% of patients after first cycle of CRF. The incidence and severity of adverse effects is less and the procedure is better tolerated by the patients.
Subject(s)
Humans , Follow-Up Studies , Hypesthesia , Incidence , Mastication , Reflex , Research Personnel , Trigeminal Ganglion , Trigeminal NeuralgiaABSTRACT
Endoplasmic reticulum (ER) stress is involved in many neurological diseases and inflammatory responses. Inflammatory mediators induce neuronal damage and trigger the neuropathic or inflammatory pain. But there is very little data on the role of the ER stress response in pain mechanisms. In this study, we explored whether the ER stress response is involved in orofacial inflammatory pain by using a complete Freund's adjuvant (CFA)-injected rat model. The thermal pain hypersensitivity increased significantly after CFA injection. We found that the protein and mRNA levels of ER stress response genes, GRP78/Bip and p-eIF2alpha, increased significantly in trigeminal ganglion (TG) of CFA-injected rats compared to control animals. In immunofluorescence analysis, a significant increase of GRP78 and p-eIF2alpha immunopositive neurons was observed in CFA-injected TG compared to control TG. When we administered an ER stress modulator, salubrinal, CFA-induced thermal pain hypersensitivity was temporally reduced. Thus, our study suggests that ER stress responses in TG neurons contribute to CFA-induced inflammatory pain, and may comprise an important molecular mechanism underlying the orofacial inflammatory pain pathway.
Subject(s)
Animals , Rats , Endoplasmic Reticulum , Endoplasmic Reticulum Stress , Facial Pain , Fluorescent Antibody Technique , Freund's Adjuvant , Hypersensitivity , Models, Animal , Neurons , RNA, Messenger , Trigeminal GanglionABSTRACT
The trigeminal cave (TC) is a special channel of dura mater, which extends from the posterior cranial fossa into the posteromedial portion of the middle cranial fossa at the skull base. The TC contains the motor and sensory roots of the trigeminal nerve, the trigeminal ganglion (TG) as well as the trigeminal cistern. This study aimed to review the anatomy of the TC and TG and determine some parameters of the TC. The study comprised two subsets: A) Cadaveric dissection on 30 sagitally sectioned formalin fixed heads and B) Volume injection. We found the dura associated with TC arranged in three distinct layers. TC had relations with internal carotid artery, the cavernous sinus, the superior petrosal sinus, the apex of petrous temporal bone and the endosteal dura of middle cranial fossa. The mean volume of TC was 0.14 ml. The mean length and breadth of TG were 18.3 mm and 7.9 mm, respectively, mean width and height of trigeminal porus were 7.9 mm and 4.1 mm, respectively, and mean length of terminal branches from TG to point of exit within skull was variable. An understanding of the precise formation of the TC, TG, TN and their relations is important in order to perform successful surgical procedures and localized neural block in the region of the TC.
El cavo trigeminal (CT) de la duramadre es un conducto especial que se extiende desde la fosa craneal posterior a la parte posteromedial de la fosa craneal media en la base del cráneo. El CT contiene las raíces motoras y sensoriales del nervio trigémino (NT), ganglio trigeminal (GT), así como la cisterna trigeminal. Este estudio tuvo como objetivo examinar la anatomía del CT y GT y para determinar algunos parámetros del CT. El estudio se realizó en dos etapas: A) la disección anatómica de 30 cabezas seccionadas sagitalmente y B) la inyección para estimar volumen. Fueron encontrados tres capas distintas de duramadre asociadas al CT. El CT se relacionó con la arteria carótida interna, el seno cavernoso, el seno petroso superior, el vértice de la porción petrosa del hueso temporal y la dura endosteal de la fosa craneal media. El volumen medio del CT fue de 0,14 ml. La longitud media y la amplitud del GT fueron 18,3 mm y 7,9 mm, respectivamente. La media del ancho y alto del poro trigeminal fueron 7,9 mm y 4,1 mm, respectivamente; la longitud media de las ramas terminales del GT al salir del cráneo fue variable. El conocimiento preciso de la formación del CT, GT, NT y sus relaciones es necesario para realizar procedimientos quirúrgicos exitosos o el bloqueo nervioso localizado en la región del CT.
Subject(s)
Humans , Cranial Fossa, Middle/innervation , Trigeminal Nerve/anatomy & histologyABSTRACT
Orofacial pain is a prevalent symptom in modern society. Some musculoskeletal orofacial pain is caused by temporomandibular disorders (TMDs). This condition has a multi-factorial etiology, including emotional factors and alteration of the masticator muscle and temporomandibular joints (TMJs). TMJ inflammation is considered to be a cause of pain in patients with TMD. Extracellular proteolytic enzymes, specifically the matrix metalloproteinases (MMPs), have been shown to modulate inflammation and pain. The purpose of this investigation was to determine whether the expression and level of gelatinolytic activity of MMP-2 and MMP-9 in the trigeminal ganglion are altered during different stages of temporomandibular inflammation, as determined by gelatin zymography. This study also evaluated whether mechanical allodynia and orofacial hyperalgesia, induced by the injection of complete Freund's adjuvant into the TMJ capsule, were altered by an MMP inhibitor (doxycycline, DOX). TMJ inflammation was measured by plasma extravasation in the periarticular tissue (Evans blue test) and infiltration of polymorphonuclear neutrophils into the synovial fluid (myeloperoxidase enzyme quantification). MMP expression in the trigeminal ganglion was shown to vary during the phases of the inflammatory process. MMP-9 regulated the early phase and MMP-2 participated in the late phase of this process. Furthermore, increases in plasma extravasation in periarticular tissue and myeloperoxidase activity in the joint tissue, which occurred throughout the inflammation process, were diminished by treatment with DOX, a nonspecific MMP inhibitor. Additionally, the increases of mechanical allodynia and orofacial hyperalgesia were attenuated by the same treatment.