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1 Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada
* To whom correspondence should be addressed. E-mail: wilsonr{at}ucalgary.ca.
The ventilatory response to several minutes of hypoxia consists of various time-dependent phenomena, some of which occur during hypoxia (e.g., short-term depression) while others appear upon returning to normoxia (e.g., post-hypoxic frequency decline). Additional phenomena can be elicited by acute, intermittent hypoxia (e.g., progressive augmentation, long-term facilitation). Current data suggest these phenomena originate centrally. We tested the hypothesis that carotid body afferent activity undergoes time-dependent modulation, consistent with a direct role in these ventilatory phenomena. Using an in vitro rat carotid body preparation, we found that: (a) Afferent activity declined during the first 5 minutes of severe (40 Torr PO2), moderate (60 Torr PO2) or mild (80 Torr PO2) hypoxia. (b) Upon returning to normoxia (100 Torr PO2) after several minutes of moderate or severe hypoxia, afferent activity was transiently reduced compared to pre-hypoxic levels (c) With successive 5-minute bouts of mild, moderate or severe hypoxia, afferent activity during bouts increased progressively. We call these phenomena, sensory hypoxic decline, sensory post-hypoxic decline and sensory progressive augmentation, respectively. These phenomena were stimulus specific: similar phenomena were not seen with 5-min bouts of normoxic hypercapnia (100 Torr PO2 & 50-60 Torr PCO2) or hypoxic hypocapnia (60 Torr PO2 & 30 Torr PCO2). However, bouts of either normoxic hypercapnia or hypocapnic hypoxia resulted in sensory long-term facilitation (sLTF). We suggest time-dependent carotid body activity acts in parallel with central mechanisms to shape the dynamics of ventilatory responses to respiratory chemostimuli.
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