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Inspiration‐Promoting Vagal Reflex in Anaesthetized Rabbits after Rostral Dorsolateral Pons Lesions
Author(s) -
Takano Kazuo,
Kato Fusao
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.042200
Subject(s) - pons , vagus nerve , reflex , stimulation , nmda receptor , brainstem , pulmonary stretch receptors , medicine , neuroscience , medulla oblongata , anesthesia , chemistry , central nervous system , receptor , biology
The centrally generated respiratory rhythm is under strong modulation by peripheral information, such as that from the slowly adapting pulmonary stretch receptors (SA‐PSRs) conveyed via the vagus nerve. We have already demonstrated that vagal afferent stimulation at a low frequency (5–40 Hz), or holding the lung volume at the end‐expiratory level (no‐inflation test) prevents spontaneous termination of the inspiratory (I) phase or initiates I activity in anaesthetized rabbits in which the NMDA receptors (NMDA‐Rs) are pharmacologically blocked. Here we show that this I‐promoting vagal reflex also becomes manifest in animals where the pontine respiratory groups are ablated. Following lesions of the rostral dorsolateral pons, including the nucleus parabrachialis medialis and Kölliker‐Fuse nucleus, with radio‐frequency current or local injection of kainic acid, low‐frequency stimulation of the vagus nerve and the no‐inflation test significantly prolonged the I phase in a manner highly similar to that observed in rabbits with NMDA‐R block. Brief stimuli at low frequency during the mid‐expiratory (E) phase evoked I discharge with a latency significantly smaller and less variable than that before the lesions. It is concluded that low‐frequency input from the SA‐PSR suppresses I‐to‐E phase transition and promotes central I activity when the medullary respiratory network is released from pontine influence, which involves NMDA‐R‐mediated signalling.