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1 Pediatrics, University of Louisville, Louisville, KY, USA; Pharmacology and Toxicology, University of Louisville, Louisville, KY, USA
2 Department of Comparative Biosciences, University of Wisconsin, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: david.gozal{at}louisville.edu.
Acute isocapnic intermittent hypoxia elicits a time-dependent, serotonin-dependent enhancement of phrenic motor output in anesthetized rats, i.e., phrenic long-term facilitation (pLTF). In adult rats, pLTF is enhanced by chronic intermittent hypoxia (CIH). To test the hypothesis that early postnatal CIH induces persistent modifications of ventilation and pLTF, male Sprague-Dawley rat pups were exposed as of the 1st day of life to a CIH profile consisting of alternating room air and 10% oxygen every 90 sec for 30 days during daylight hours (RAIH), or to a comparable exposures consisting of room air throughout (RARA). One month after cessation of CIH, respiratory responses were recorded using whole-body plethysmography and integrated phrenic nerve activity was recorded in urethane-anaesthetized, vagotomized, paralyzed and ventilated rats at baseline and following exposures to three, 5-min hypoxic episodes (FIO2 = 0.11) separated by 5 min hyperoxia (FIO2 = 0.5). RAIH rats displayed greater normoxic ventilation and also increased burst frequency compared to RARA rats (p<0.01). Ventilatory responses to hypoxia and short-term phrenic responses during acute hypoxic challenges were reduced in RAIH (p<0.01). Although pLTF was present in both RAIH and RARA rats, it was diminished in RAIH (minute activity: 74±2% in RARA vs. 55±5% in RAIH rats at 60 min; p<0.01). Thus, we conclude that early postnatal CIH modifies normoxic and hypoxic ventilatory and phrenic responses that persist at one month after cessation of CIH (i.e., metaplasticity), and markedly differ from previously reported increased neural plasticity changes induced by CIH in adult rats.
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