歯根膜ルフィニ神経終末の再生過程におけるASIC3発現様式の変化)

学位の種類: 博士（歯学）. 報告番号: 甲第3879号. 学位記番号: 新大院博（歯）甲第298号. 学位授与年月日: 平成26年3月24日The acid-sensing ion channel 3 (ASIC3), belonging to the epithelial sodium-channel/degenerin (ENaC/DEG) superfamily, is regarded as an essential ion channel for mechanosensation. Our recent study has confirmed the expression of ASIC3 in the mechanoreceptive Ruffini endings in the periodontal ligament of mice incisors, indicating that this molecule is a new marker for mechanoreceptors. Although the periodontal Ruffini endings have been reported to have a potential for high neuroplasticity, no information is available regarding the role of ASIC3 during the regeneration process after nerve injury. This study was therefore undertaken to examine changes in the expression pattern of ASIC3 in the periodontal ligament and trigeminal ganglion of the rats. After transection of the inferior alveolar nerve (IAN), cryostat sections -- including the lingual ligament of the lower incisors and trigeminal ganglia -- were processed for immunohistochemical procedures. As previously reported, the periodontal Ruffini endings disappeared on postoperative (PO) Day 3, and began regeneration from PO Day 7 to return to their normal morphology by PO Day 28, as shown by immunohistochemistry for protein gene product 9.5, a neuronal marker. However, no apparent immunoreaction for ASIC3 was ever recognizable in the periodontal ligament throughout this observation period. On the other hand, a strong immunoreaction for ASIC3 occurred in the satellite cells encircling the trigeminal ganglion neurons on the ipsilateral side. These findings indicate that ASIC3 is not directly involved in the axonal regeneration of the periodontal Ruffini endings but rather in neuron-glial interactions such as control of the neuronal activity in the trigeminal ganglion.博士（歯学）新潟大