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1 Department of Physiology and Pharmacology, Bristol Heart Institute, University of Bristol, Bristol, United Kingdom
2 Department of Neurobiology & Anatomy, Drexel University College of Medicine, Philadelphia, PA
3 Cellular and Systems Neurobiology Section, Laboratory of Neural Control, NINDS, NIH, Bethesda, MD
ABSTRACT
We have focused on brainstem regions and mechanisms involved in generating expiratory activity. We recorded phrenic (PN), central vagus (cVN) and AB outflow (T10-L1) during hypercapnia, following brainstem transections and chemical suppression of the retrotrapezoid nuclei (RTN) & parafacial (PF). In the in situ decerebrate preparation of rat, AB expiratory activity exhibited low amplitude post-inspiratory (post-I) discharge. In hypercapnia (7–10% CO2) augmenting late-expiratory (late-E) discharge was evoked. Sectioning the rostral pons revealed a 2-phase rhythm with tonic AB discharge throughout expiration. When the BötC was removed all expiratory activity was abolished and could not be reinstated by hypercapnia (n=7). Suppression of RTN/PF (isoguvacine, 60 nL, 20 mM) attenuated resting post-I activity in AB (–69±14 %, n=5, P<0.05) and cVN (–68±12 %, n=5, P<0.05), which partially recovered in hypercapnia, and abolished late-E AB bursts evoked by hypercapnia (n=5). The most effective sites were localised in the caudal half of RTN/PF. We conclude that the integrity of RTN/PF is required for regeneration late-E AB bursts during hypercapnia. The BötC is essential for generation of expiratory activity for the 2-phase rhythm. The pons provides essential tonic excitatory drive to post-I cell populations in the brainstem with RTN/PF contributing to this drive. Support: NIH-RO1 NS057815.
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