Mylohyoid discharge of the in situ rat: a probe of pontile respiratory activities in eupnea and gasping

• Published in: Journal of applied physiology (1985) Vol. 108; no. 3; pp. 614 - 620
• Main Authors: JOHN, Walter M. St, RUDKIN, Alison H, LEITER, J. C
• Format: Journal Article
• Language: English
• Published: Bethesda, MD American Physiological Society 01.03.2010
• Subjects: Action Potentials; Animals; Biological and medical sciences; Biological Clocks; Brain; Brain Ischemia - physiopathology; Carotid Sinus - innervation; Decerebrate State; Disease Models, Animal; Fundamental and applied biological sciences. Psychology; Hypercapnia - physiopathology; Hypoxia; Hypoxia - physiopathology; Mandibular Nerve - physiopathology; Neurons; Perfusion; Periodicity; Phrenic Nerve - physiopathology; Pons - physiopathology; Rats; Respiratory Mechanics; Respiratory system; Rodents; Time Factors; Vagotomy; Vagus Nerve - surgery; medulla; Breathing rate; Rat; Brain stem; In situ; Rodentia; Central nervous system; respiratory rhythm generation; Discharge; Encephalon; pons; Vertebrata; Mammalia
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00988.2009

Our purpose was to characterize respiratory-modulated activity of the mylohyoid nerve. Since its motoneurons are in the trigeminal motor nucleus, mylohyoid discharge could serve as a probe of the role of pontile mechanisms in the generation of respiratory rhythms. Studies were performed in the decerebrate, perfused in situ preparation of the rat. Phrenic discharge was recorded as the index of the respiratory rhythm. In eupnea, the mylohyoid nerve discharged primarily during neural expiration, in the period between phrenic bursts. This expiratory discharge increased greatly in hypoxia and fell in hypercapnia. The hypoxia-induced increase in mylohyoid discharge was due, at least in part, to a direct influence of hypoxia on the brain stem. In ischemia, phrenic discharge increased, and then declined to apnea, which was succeeded by gasping. The mylohyoid nerve discharged tonically during the apneic period, but still declined during each of the phrenic bursts of gasping. This maintenance of a respiratory-modulation of the mylohyoid discharge in gasping supports the concept that a release of medullary mechanisms, rather than a ubiquitous suppression of pontile influences, underlies the neurogenesis of gasping. Results also provide additional support for our conclusion that activity of any single cranial nerve does not provide an accurate index of the type of respiratory rhythm, be it eupnea or gasping.