2018 Fiscal Year Final Research Report

Trigeminal nerve transection-induced neuroplastic changes in the somatosensory and insular cortices in a rat ectopic pain model

Research Project

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Project/Area Number	16H05507
Research Category	Grant-in-Aid for Scientific Research (B)
Allocation Type	Single-year Grants
Section	一般
Research Field	Functional basic dentistry
Research Institution	Nihon University
Principal Investigator	KOBAYASHI Masayuki 日本大学, 歯学部, 教授 (00300830)
Co-Investigator(Kenkyū-buntansha)	藤田智史日本大学, 歯学部, 准教授 (00386096) 山本清文日本大学, 歯学部, 助教 (30609764) 崔翼龍国立研究開発法人理化学研究所, ライフサイエンス技術基盤研究センター, ユニットリーダー (60312229)
Project Period (FY)	2016-04-01 – 2019-03-31
Keywords	疼痛 / 神経損傷 / 大脳皮質 / 島皮質 / 神経可塑性 / 光学計測 / カルシウム測光 / 抑制性シナプス後電流
Outline of Final Research Achievements	To elucidate the mechanisms of neuropathic pain and allodynia in the central nervous system, we focused on plastic changes of excitation in secondary somatosensory cortex and insular oral region (S2/IOR) of inferior alveolar nerve transection (IANX) model rats in which the mandibular but not maxillary nerve branch was cut. Optical imaging using VSD revealed contradictory excitatory responses 1 w after IANX between mandibular and maxillary molar pulp stimulation as follows: the loss of excitation following mandibular stimulation vs facilitated excitation following maxillary stimulation. At this stage, the neural activities in layer II/III excitatory and inhibitory neurons in S2/IOR in the IANX model rats were enhanced due to facilitated glutamatergic inputs. On the other hand, the inhibitory inputs onto the pyramidal neurons were reduced in the IANX model rats. These results suggest that IANX induces plastic changes in S2/IOR by changing the local excitatory and inhibitory circuits.
Free Research Field	神経生理学
Academic Significance and Societal Importance of the Research Achievements	口腔領域は，触圧覚や味覚，歯根膜感覚など多様な感覚入力が同時に生じる点が，他の感覚と大きく異なる。本研究によって明らかになった現象，すなわち下顎からの感覚入力遮断による上顎歯髄刺激応答の増大は，味覚や温度感覚，筋感覚など島皮質が司っている他の感覚との相互作用を起こす可能性を示唆するものである。さらに，このような現象には大脳皮質の回路の再編が含まれていることから，末梢組織の損傷からの回復後に生じる慢性的な異常疼痛のメカニズムに中枢神経系が関与することが明らかとなった。この成果は，今後，臨床で生じる様々な感覚異常の治療法の開発に貢献すると期待できる。