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Dental Journals | Dentistry Journals | Oral Health | High Impact Articles | Scient Open Access
Journal of Dental and Oral Health


Research Article

Astrocyte Activation in the Brainstem Evoked by Inflammatory Stimulation of the Masticatory Muscle

Shunji KUMABE, Michiko NAKATSUKA, Ji-Youn KIM, Chizuko INUI-YAMAMOTO, Koichiro JIN, Seong-Suk JUE, Je-Won SHIN, Isao TAMURA

Correspondence Address :

Michiko Nakatsuka
Department of Oral Health Engineering
Osaka Dental University Faculty of Health Sciences
Tel: +81-72-856-9964
Fax: +81-72-856-9952

Received on: October 10, 2017, Accepted on: October 25, 2017, Published on: October 31, 2017

Citation: Shunji KUMABE, Michiko NAKATSUKA, Ji-Youn KIM, et al. (2017). Astrocyte Activation in the Brainstem Evoked by Inflammatory Stimulation of the Masticatory Muscle

Copyright: 2017 Michiko Nakatsuka, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

  • Abstract

Objective: To identify a suitable treatment for masticatory muscle pain disorder, two stimuli were provided to the masseter muscle to cause inflammation, and the time course of changes in the number of astrocytes in the brainstem was determined.
Materials and Methods: A solution of 50 μl of lipopolysaccharide (LPS, 2 μg/kg) dissolved in saline was administered to the left masseter muscle (LMM) of Sprague-Dawley rats. After 24 h of recovery, the experimental group received 50 μl of a 6% sodium chloride solution 5 times every 90 min and the control group received another 50 μl of the LPS solution (2 μg / kg) dissolved in saline. The LMM and brainstem were dissected 1, 3, or 7 days after administering the reagents, and frozen sections were prepared. The expression of tumor necrosis factor α (TNFα) and bradykinin receptor B2 (BKRB2) in the masseter muscle and of an astrocytic marker and phosphorylated extracellular signal-regulated kinase (pERK) in the brainstem was examined by immunohistochemical staining.
Results: The expression of TNFα and BKRB2 in the LMM markedly increased 1 day after stimulation in the experimental and control groups, but the levels returned to nearly normal 7 days after stimulation. In the trigeminal subnucleus caudalis (Vc), there was a marked increase in the number of glial fibrillary acidic protein (GFAP) and pERK-immunoreactive (IR) cells 7 days after stimulation in the experimental group. pERK-IR cells were observed in the dorsomedial, laterodorsal and central regions of the Vc. Conclusions: When inflammation in the masticatory muscle was induced by the administration of LPS, which is an inflammatory factor, and a 6% sodium chloride solution, which is an infringing factor, activated astrocytes and pERK in the Vc persisted for around 1 week, even after local inflammation had subsided, which suggests a transition to chronic pain.
Keywords: Masseter, Glia, Inflammation