2016 Fiscal Year Final Research Report
Analysis of neuronal mechanisms underlying glossoptosis using arterially perfused decerebrate rats
Project/Area Number |
15K15687
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Functional basic dentistry
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Research Institution | Showa University |
Principal Investigator |
INOUE TOMIO 昭和大学, 歯学部, 教授 (70184760)
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Project Period (FY) |
2015-04-01 – 2017-03-31
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Keywords | 舌筋 / 呼吸 / 動脈灌流標本 / 上気道開大筋 / 二酸化炭素負荷 |
Outline of Final Research Achievements |
Glossoptosis may cause obstructive ventilatory defects, such as obstructive sleep apnea syndrome; however, its etiology is not clear. In this study, we analyzed effects of hypercapnic acidosis on the respiratory motor nerve activity innervating the upper airway muscles using arterially perfused decerebrate rats. During hypercapnic acidosis (8% CO2), the peak amplitudes of the inspiratory discharges in the cervical spinal nerve innervating the infrahyoid muscles (CN), the hypoglossal nerve (HGN), the external branch of the superior laryngeal nerve (SLN), and the recurrent laryngeal nerve (RLN) were increased. Moreover, hypercapnic acidosis induced pre-inspiratory discharges in the CN, HGN, SLN, and RLN. These results suggest that the securing of the airway that occurs a certain time before dilation of the glottis may facilitate ventilation and improve hypercapnic acidosis. Glossoptosis may occur due to some defects of such regulation of upper airway muscle activity.
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Free Research Field |
吸啜、咀嚼、嚥下を中心とした摂食行動の神経生理
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