Premium
Hypercapnic ventilatory response of adult quail after chronic neonatal hypercapnia
Author(s) -
Foster Jennifer A.,
Broge Thomas A.,
Atchley Dylan S.,
Bavis Ryan W.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.955.10
Subject(s) - hypercapnia , quail , ventilation (architecture) , medicine , hypoxic ventilatory response , hatching , control of respiration , anesthesia , endocrinology , respiratory system , biology , zoology , mechanical engineering , engineering
Embryonic exposure to 2% CO 2 attenuates the hypercapnic ventilatory response (HCVR) of adult female Japanese quail ( Coturnix japonica ) by ~40% (Bavis & Kilgore, Respir. Physiol. 126:183–199, 2001); this treatment does not alter the HCVR of males. The present study investigated whether chronic hypercapnia during the neonatal period elicits similar developmental plasticity. Quail were exposed to 5% CO 2 from hatching through 14–17 days of age; a control group was raised in air. Once sexually mature (6–9 weeks of age), the HCVR was measured by barometric plethysmography for quail acutely exposed to 6% CO 2 (n=13–17 per sex per treatment group). Neonatal hypercapnia had no lasting effect on baseline ventilation. When HCVR is calculated as absolute ventilation during 6% CO 2 or as the absolute increase in ventilation from baseline, HCVR was reduced by ~20% in females exposed to neonatal hypercapnia whereas males were unchanged (treatment × sex, P <0.05). Despite a similar trend, HCVR was not significantly reduced when calculated as a percentage of baseline ventilation or when ventilation is normalized to metabolic rate. Together, these data suggest that chronic neonatal hypercapnia has only minor effects on the adult HCVR in quail. Thus, the critical period for this developmental plasticity appears to lie primarily within the embryonic period for this precocial species. Supported by NIH grant P20 RR‐016463 (Maine INBRE).