Developmental hyperoxia attenuates the hypoxic ventilatory response in Japanese quail (Coturnix japonica)

Abstract

Early life experiences can influence development of the respiratory control system. We hypothesized that chronic hyperoxia (60% O 2 ) during development would attenuate the hypoxic ventilatory response (HVR) of Japanese quail (Coturnix japonica), similar to the effects of developmental hyperoxia in mammals. Quail were exposed to hyperoxia during prenatal development, during postnatal development, or during both prenatal and postnatal development (for approximately 2 or 4 weeks). HVR (11% O 2 ) was subsequently assessed in adults (>6 weeks old) via barometric plethysmography and compared to quail raised in normoxia (i.e., control). The HVR of quail exposed to hyperoxia both prenatally and postnatally was reduced 50-60% compared to control quail whereas postnatally exposed quail exhibited normal HVR. The effects of prenatal hyperoxia on HVR were equivocal and depended on how HVR was expressed. We conclude that developmental exposure to 60% O 2 attenuates the HVR in quail and that the critical period for this plasticity encompasses the late prenatal and early postnatal periods.

Chronic hyperoxia and the development of the carotid body

“…Subsequent studies revealed that the critical period for long-lasting changes in the HVR is limited to the first two postnatal weeks in rats (Bavis et al, 2002). It is now known that developmental hyperoxia has similar effects on the HVR in several vertebrates species, including mice (Bavis et al, 2011a), quail (Bavis & Simons, 2008), chickens (Mortola, 2011), and zebrafish (Vulesevik and Perry, 2006); while fish do not have a carotid body per se , they have O 2 -sensitive chemoreceptors in their gills that are considered homologous to those in the mammalian and avian carotid body (Milsom and Burleson, 2007). No controlled experiments have been conducted in human infants, but there is correlative evidence suggesting that ventilatory control is affected by supplemental O 2 in humans as well (Calder et al, 1994; Katz-Salamon and Lagercrantz, 1994; Katz-Salamon et al, 1996).…”

“…Egg-laying species have been used to circumvent these obstacles since environmental O 2 levels of developing embryos can be controlled in incubators (i.e., prenatal = pre-hatching). Like mammals, quail (Bavis and Simons, 2008) and chickens (Mortola, 2011) exhibited blunted HVR following developmental hyperoxia, and these effects may persist into adulthood (Bavis and Simons, 2008); hypercapnic ventilatory responses were unaffected (Mortola, 2011). It is likely that the diminished HVR in these birds is explained by abnormal carotid body function, although this has not been tested directly.…”

“…It is likely that the diminished HVR in these birds is explained by abnormal carotid body function, although this has not been tested directly. Importantly, chicken embryos were exposed to hyperoxia (40 or 60% O 2 ) for the last week of incubation through hatching, and quail were exposed to hyperoxia (60% O 2 ) for 2–4 weeks spanning both the prenatal and postnatal periods or only during the prenatal period; quail exposed to hyperoxia primarily during postnatal development exhibited normal HVR (Bavis and Simons, 2008). Thus, these findings suggest that the critical period for hyperoxia-induced plasticity extends prenatally in these precocial bird species.…”