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1 Institute of Arctic Biology, University of Alaska Fairbanks, Fairbanks, AK, USA; Department of Physiology, Dartmouth Medical School, Dartmouth Medical School, Lebanon, NH, USA
2 Department of Physiology, Dartmouth Medical School, Dartmouth Medical School, Lebanon, NH, USA
* To whom correspondence should be addressed. E-mail: ffmbh{at}uaf.edu.
The perfused in situ juvenile rat preparation produces patterns of phrenic discharge comparable to eupnea and gasping in vivo. These ventilatory patterns differ in multiple aspects including, most prominently the rate of rise of inspiratory activity. Although we have recently demonstrated that both eupnea and gasping are similarly modulated by a Hering-Breuer expiratory-promoting reflex to tonic pulmonary stretch, it has generally been assumed that gasping was unresponsive to afferent stimuli from pulmonary stretch receptors. In the present study, we record eupneic and gasp-like efferent activity of the phrenic nerve in the in situ juvenile rat perfused brainstem preparation, with and without phrenic-triggered phasic pulmonary inflation. We test the hypothesis that phasic pulmonary inflation produces reflex responses in situ akin to those in vivo, and that both eupnea and gasping are similarly modulated by phasic pulmonary stretch. In eupnea, we found that phasic pulmonary inflation decreases inspiratory burst duration and the period of expiration, thus increasing burst frequency of the phrenic neurogram. Phasic pulmonary inflation also decreases the duration of expiration and increases the burst frequency during gasping. Bilateral vagotomy eliminated these changes. We conclude that the neural substrate mediating the Hering-Breuer reflex is retained in the in situ preparation, and that that the brainstem circuitry generating the respiratory patterns respond to phasic activation of pulmonary stretch receptors in both eupnea and gasping. These findings support the homology of eupneic phrenic discharge patterns in the reduced in situ preparation and eupnea in vivo, and disprove the common supposition that gasping is insensitive to vagal afferent feedback from pulmonary stretch receptor mechanisms.
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