- 著者
- Shinji Okada Ayano Katagiri Hiroto Saito Jun Lee Kinuyo Ohara Toshimitsu Iinuma Koichi Iwata
- 出版者
- Nihon University School of Dentistry
- 雑誌
- Journal of Oral Science (ISSN:13434934)
- 巻号頁・発行日
- vol.61, no.2, pp.370-378, 2019 (Released:2019-06-18)
- 参考文献数
- 40
- 被引用文献数
- 10
Peripheral nerve injury can induce neuroplastic changes in the central nervous system and result in neuropathic pain. This study investigated functional involvement in dorsal paratrigeminal nucleus (dPa5) and nucleus tractus solitarii (NTS) neurons projecting to the parabrachial nucleus (PBN) after trigeminal nerve injury. Anatomical quantification was performed based on phosphorylated extracellular signal-regulated kinase (pERK) expression underlying orofacial neuropathic pain associated with infraorbital nerve chronic constriction injury (ION-CCI) in rats. ION-CCI rats exhibited heat and mechanical hypersensitivity in the ipsilateral upper lip. After injection of retrograde tracer fluorogold (FG) into the contralateral PBN, ION-CCI rats received capsaicin or noxious mechanical stimulation to the upper lip. The total number of FG-labeled neurons in dPa5 and NTS did not change after ION-CCI, and pERK expression in dPa5 did not differ between sham and ION-CCI rats. In the NTS contralateral to ION-CCI, the number of pERK-immunoreactive neurons and percentage of pERK-immunoreactive FG-labeled PBN projection neurons were increased after capsaicin stimulation in ION-CCI rats. The present findings suggest that enhanced noxious inputs from the NTS to the PBN after trigeminal nerve injury modulates PBN neuron activity, which accompanies the affective components of orofacial neuropathic pain.
- 著者
- Shinji Okada Hiroto Saito Yutaka Matsuura Lou Mikuzuki Shiori Sugawara Hiroki Onose Junichi Asaka Kinuyo Ohara Jun Lee Toshimitsu Iinuma Ayano Katagiri Koichi Iwata
- 出版者
- Nihon University School of Dentistry
- 雑誌
- Journal of Oral Science (ISSN:13434934)
- 巻号頁・発行日
- vol.61, no.1, pp.146-155, 2019 (Released:2019-03-28)
- 参考文献数
- 77
- 被引用文献数
- 2
Bright light stimulation of the eye activates trigeminal subnucleus caudalis (Vc) neurons in rats. Sensory information is conveyed to the Vc via the trigeminal ganglion (TG). Thus, it is likely that TG neurons respond to photic stimulation and are involved in photic hypersensitivity. However, the mechanisms underlying this process are unclear. Therefore, the hypothesis in this study is bright light stimulation enhances the excitability of TG neurons involved in photic hypersensitivity. Expressions of calcitonin gene-related peptide (CGRP) and neuronal nitric oxide synthase (nNOS) were significantly higher in TG neurons from 5 min to 12 h after photic stimulation of the eye. Phosphorylation of extracellular signal-regulated kinase1/2 (pERK1/2) was enhanced in TG neurons within 5 min after photic stimulation, while pERK1/2 immunoreactivity in satellite glial cells (SGCs) persisted for more than 12 h after the stimulus. Activation of SGCs was observed from 5 min to 2 h. Expression of CGRP, nNOS, and pERK1/2 was observed in small and medium TG neurons, and activation of SGCs and pERK1/2-immunoreactive SGCs encircling large TG neurons was accelerated after stimulation. These results suggest that upregulation of CGRP, nNOS, and pERK1/2 within the TG is involved in photic hypersensitivity.
- 著者
- Tetsuro Watase Kohei Shimizu Hiroki Komiya Kinuyo Ohara Koichi Iwata Bunnai Ogiso
- 出版者
- Nihon University School of Dentistry
- 雑誌
- Journal of Oral Science (ISSN:13434934)
- 巻号頁・発行日
- pp.16-0854, (Released:2018-02-26)
- 参考文献数
- 21
- 被引用文献数
- 9
A study was conducted to evaluate the mechanisms underlying ectopic orofacial pain associated with tooth pulp inflammation in rats. We observed a significant decrease in the head withdrawal threshold (HWT) response to mechanical and heat stimuli applied to the ipsilateral facial skin upon application of complete Freund’s adjuvant (CFA) to the upper first molar (M1TP) in comparison to application of vehicle. A large number of trigeminal ganglion (TG) neurons showed transient receptor potential vanilloid 1 (TRPV1) immunoreactivity (IR), and some of them were retrogradely labeled with fluorogold injected into the facial skin. A large number of cells showing IR for glial fibrillary acidic protein (GFAP) were observed in the 2nd compared to the 1st or 3rd branch regions of the TG, and TG cells innervating the facial skin were also surrounded by GFAP-IR cells. After administration of TRPV1 antagonist into the facial skin of M1TP CFA-treated rats, the decrease of HWTs in response to mechanical and heat stimulation of the facial skin was significantly reversed. The present findings suggest that the excitability of TG neurons is enhanced upon tooth pulp inflammation, leading to overexpression of TRPV1 in TG neurons innervating the facial skin, and that satellite glial cells are also activated, resulting in the development of ectopic orofacial pain.