• Journal of the korean academy of Pediatric Dentistry
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• v.25 no.1
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• pp.249-256
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• 1998

Glial fibrillary acidic proteins (GFAP) are a group of intermediate filaments that are distributed in the cytoplasm of glial cells. GFAP immunoreactivity (GFAP-IR) increase after central and peripheral nerve injuries. The purpose of this study was to determine change of GFAP-IR in rat trigeminal ganglion satellite cells following the axotomy of inferior alveolar nerve(IAN). The immunohistochemistry was carried out using the avidin-biotin-peroxidase complex(ABC) method. 1. Control group : Astrocytes in central root of trigeminal ganglion had strong GFAP-IR, but satellite cells of trigeminal ganglion occasionally had GFAP-IR. The patterns of reactivity in satellite cells of trigeminal ganglion were not concenturated in any specific region of trigeminal ganglion. 2. Three day group after IAN axotomy : There were highly GFAP-IR in satellite cells of trigeminal ganglion in mandibular region. GFAP-IR in maxillary and ophthalmic regions were less intense compared to mandibular region. 3. Seven day group after IAN axotomy : GFAP-IR that were increased compared to control group were seen in the mandibular region. But GFAP-IR were less intense compared to three day group. These results suggest that GFAP-IR increase in specific region of trigeminal ganglion following peripheral axotomy. therefore we suppose that GFAP study offer research tool in trigeminal neuralgia.

• International Journal of Oral Biology
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• v.34 no.3
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• pp.157-164
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• 2009

We recently described a novel animal model of trigeminal neuropathic pain following compression of the trigeminal ganglion (Ahn et al., 2009). In our present study, we adapted this model using male Sprague-Dawley rats weighing between 250-260 g and then analyzed the behavioral responses of these animals following modified chronic compression of the trigeminal ganglion. Under anesthesia, the rats were mounted onto a stereotaxic frame and a 4% agar solution ($10{\mu}L$) was injected in each case on the dorsal surface of the trigeminal ganglion to achieve compression without causing injury. In the control group, the rats received a sham operation without agar injection. Air-puff, acetone, and heat tests were performed at 3 days before and at 3, 7, 10, 14, 17, 21, 24, 30, 40, 55, and 70 days after surgery. Compression of the trigeminal ganglion produced nociceptive behavior in the trigeminal territory. Mechanical allodynia was established within 3 days and recovered to preoperative levels at approximately 60 days following compression. Mechanical hyperalgesia was also observed at 7 days after compression and persisted until the postoperative day 40. Cold hypersensitivity was established within 3 days after compression and lasted beyond postoperative day 55. In contrast, compression of the trigeminal ganglion did not produce any significant thermal hypersensitivity when compared with the sham operated group. These findings suggest that compression of the trigeminal ganglion without any injury produces prolonged nociceptive behavior and that our rat model is a useful system for further analysis of trigeminal neuralgia.

• Restorative Dentistry and Endodontics
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• v.22 no.2
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• pp.782-791
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• 1997

Glial fibrillary acidic protein(GFAP) are a group of intermediate filaments that are distributed in the cytoplasm of many type of glial cells. The purpose of this study was to determine change of GFAP immunoreactivity(GFAP-IR) in rat trigeminal ganglion satellite cells in response to pulp exposure. The immunohistochemistry was carried out using the avidinbiotin-peroxidase complex(ABC) method and subsequently stained with AEC(3-aminoethyl-9-carbasol). 1. Contol group; Central root astrocytes had strong GFAP-IR, but ganglion satellite cells occasionlly had GFAP-IR. This reaction patterns of ganglion satellite cells was not concenturated in any specific region of trigeminal ganglion. 2. Three day pulp exposure group; There was a highly GFAP-IR in satellite cells of trigeminal ganglion in maxillary region. GFAP-IR in neighboring mandibular and ophthalmic regions was less intense compared to maxillary region. 3. Seven day pulp exposure group; In this group, GFAP-IR that was increased compared to control group was seen in the maxillary region. But GFAP-IR was less intense compared to three day pulp exposure group. These results suggest that GFAP in satellite cell increase in specific region of trigeminal ganglion after pulp exposure and offer useful tool in trigeminal pain research.

• International Journal of Oral Biology
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• v.33 no.4
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• pp.155-162
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• 2008

The present study investigated inflammatory hypersensitivity following compression of the trigeminal ganglion in rats. Experiments were carried out on male Sprague-Dawley rats weighing 250-260 g. Under anesthesia, rats were mounted on a stereotaxic frame and injected with $8{\mu}L$ of 4% agar solution through a stainless steel injector to compress the trigeminal ganglion. In the control group, rats underwent a sham operation without agar injection. Injection sites were examined with a light micrograph after compression of the trigeminal ganglion. Air-puff thresholds (mechanical allodynia) were evaluated 3 days before surgery and 3, 7, 10, 14, 17, 21, 24, 30, and 40 days after surgery. Air-puff thresholds significantly decreased after compression of the trigeminal ganglion. Mechanical allodynia was established within 3 days and remained strong over 24 days, returning to preoperative levels approximately 40 days following compression. After subcutaneous injection of 5% formalin ($50{\mu}L$) in the compression of the trigeminal ganglion-treated rats, nociceptive scratching behavior was recorded for 9 successive 5-min internals. Injection of formalin into the vibrissa pad significantly increased the number of scratches and duration of noxious behavioral responses in sham-treated rats. Noxious behavioral responses induced by subcutaneous formalin administration were significantly potentiated in rats with trigeminal ganglion compression. These findings suggest that compression of the trigeminal ganglion enhanced formalin-induced infla-mmatory pain in the orofacial area.

• The Korean Journal of Pain
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• v.10 no.1
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• pp.11-15
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• 1997

Background : There are several treatment of trigeminal neuralgia including Gasserian Ganglion Block. This paper retrospectively analyze the efficacy of Gasserian Ganglion Block as main treatment of trigeminal neuralgia. Methods : We studied 55 patients for followings; sex, age, duration from onset to visit, consulted mediator, causes, characteristics of pain, affected area, types of block, kinds and volume of used neurolytic agents, duration from first block to repeat block, types of repeat block, complications, if surgery was necessary after block. Results : Characteristic items of trigeminal neuralgia are similar with other studies. Mean duration of pain relief was 23 months. The duration was shortened in the repeat block. There were no significant complication. Conclusion : Considering Gasserian Ganglion Block as main treatment of trigeminal neuralgia is an effective and safe method. Therefore we would like to recommend the need to increase public awareness of trigeminal neuralgia and its possible treatment in pain clinics through mass commanication.

• International Journal of Oral Biology
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• v.35 no.3
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• pp.75-81
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• 2010

The present study investigated the role of ERK in the onset of mechanical and cold allodynia in a rat model of compression of the trigeminal ganglion by examining changes in the air-puff thresholds and number of scratches following the intracisternal injection of PD98059, a MEK inhibitor. Male Sprague Dawley rats weighing between 250 and 260 g were used. Under anesthesia, the rats were mounted onto a stereotaxic frame and received 4% agar ($10\;{\mu}l$) solution to compress the trigeminal ganglion. In the control group, the animals were given a sham operation without the application of agar. Changes in behavior were examined at 3 days before and at 3, 7, 10, 14, 17, 21, 24, 30, and 40 days after surgery. Compression of the trigeminal ganglion significantly decreased the air-puff thresholds. Mechanical allodynia was established within 3 days and persisted over postoperative day 24. To evaluate cold allodynia, nociceptive scratching behavior was monitored after acetone application on the vibrissa pad of the rats. Compression of the trigeminal ganglion was found to produce significant cold allodynia, which persisted for more than 40 days after surgery. On postoperative day 14, the intracisternal administration of $1\;{\mu}g$ or $10\;{\mu}g$ of PD98059 in the rat model significantly decreased the air-puff thresholds on both the ipsilateral and contralateral side. The intracisternal administration of $10\;{\mu}g$ of PD98059 also significantly alleviated the cold allodynia, compared with the vehicle-treated group. These results suggest that central ERK plays an important role in the development of mechanical and cold allodynia in rats with compression of the trigeminal ganglion and that a targeted blockade of this pathway is a potential future treatment strategy for trigeminal neuralgia-like nociception.

• Biomedical Science Letters
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• v.11 no.3
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• pp.375-382
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• 2005

This study aimed to investigate whether nociceptin is implicated in the, trigeminovascular responses to electrical stimulation of trigeminal ganglion in rats. An open cranial window was prepared on the right parietal bone of male Sprague-Dawley rats. Trigeminovascular system was stimulated by electrical stimulation of trigeminal ganglion (ETS; 5ms, 5Hz, 3V). Neonatal capsaicin treatment was performed with subcutaneous administration of capsaicin (50mg/kg) within the first 24 hours after birth. Changes in regional cerebral blood flow were continuously measured through the cranial window by laser-Doppler flowmetry, and the expression of nociceptin-like immunoreactivity was determined by immunohistochemistry. ETS caused increases in regional blood flow of pial arteriole in a voltage-dependent manner. ETS markedly and voltage-dependently increased the expression of nociceptin-like immunoreactivity in dura mater ipsilateral rather than contralateral to ETS. The nociceptin-like immunoreactivity was markedly reduced by pretreatments with calcitonin gene-related peptide(8-37) ($CGRP_{8-37},\;a\;CGRP_1$ receptor antagonist), L-733060 (a $NK_1$ receptor antagonist), and $[Nphe^1]$ nociceptin(1-13)$NH_2$ (a selective and competitive nociceptin receptor antagonist) as well as by neonatal capsaicin treatment. These results suggest that the electrical stimulation of trigeminal ganglion causes prominent expression of nociceptin within dura mater, in which not only neuropeptides inducing substance P and CGRP but also nociceptin are implicated in the trigeminovascular responses to electrical trigeminal ganglion stimulation.

• Proceedings of the KACD Conference
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• 2001.11a
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• pp.581.1-581
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• 2001

Trigeminal nerve functions movement and sensation on orofacial region. Therefore, it is very important in dental clinic. Neurons with their cell bodies in trigeminal ganglion of trigeminal nerve root are primary sensory neurons and playa role of tactile sense, pressure, vibration and pain of orofacial area. Transmission of these senses depends on ion channels, we know that trigeminal ganglion neuron exists many kind of ion channels. Methods of definition on ion channel are several, but in this study we use immunostaining for detection of ion channels.(omitted)

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.33 no.3
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• pp.227-237
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• 2007

Microglial cell activation is known to contribute to neuropathic pain following spinal sensory nerve injuries. In this study, I investigated its mechanisms in the case of trigeminal sensory nerve injuries by which microglial cell and p38 mitogen-activated protein kinase (p38 MAPK) activation in the medullary dorsal horn (MDH) would contribute to the facial pain hypersensitivity following mandibular nerve transection (MNT). And also investigated the changes of trigeminal ganglion neurons and ERK, p38 MAPK manifestations. Activation of microglial cells was monitored at 1, 3, 7, 14, 28 and 60 day using immunohistochemical analyses. Microglial cell activation was primarily observed in the superficial laminae of the MDH. Microglial cell activation was initiated at postoperative 1 day, maximal at 3 day, maintained until 14 day and gradually reduced and returned to the basal level by 60 days after MNT. Pain hypersensitivity was also initiated and attenuated almost in parallel with microglial cell activation pattern. To investigate the contribution of the microglial cell activation to the pain hypersensitivity, minocycline, an inhibitor of microglial cell activation by means of p38 MAPK inhibition, was administered. Minocycline dose-dependently attenuated the development of the pain hypersensitivity in parallel with inhibition of microglial cell and p38 MAPK activation following MNT. Mandibular nerve transection induced the activation of ERK, but did not p38 MAPK in the trigeminal ganglion. These results suggest that microglial cell activation in the MDH and p38 MAPK activation in the hyperactive microglial cells play an important role in the development of facial neuropathic pain following MNT. The results also suggest that ERK activation in the trigeminal ganglion contributes microglial cell activation and facial neuropathic pain.

• Journal of Dental Anesthesia and Pain Medicine
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• v.19 no.2
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• pp.77-82
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• 2019

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.