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Carotid body growth and the critical period for hyperoxia‐induced developmental plasticity in rats
Author(s) -
Bavis Ryan W,
Fallon Sarah C,
Tobin Kristina E,
Dmitrieff Elizabeth F
Publication year - 2012
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.26.1_supplement.1090.9
Subject(s) - carotid body , hypoxic ventilatory response , hyperoxia , ventilation (architecture) , period (music) , medicine , hypoxia (environmental) , endocrinology , respiratory system , lung , chemistry , carotid arteries , mechanical engineering , physics , organic chemistry , oxygen , acoustics , engineering
Chronic postnatal hyperoxia elicits both transient and long‐lasting plasticity in the control of breathing, primarily through effects at the carotid body. We hypothesized that the critical period for long‐lasting changes to the hypoxic ventilatory response (HVR) would correspond to the period of postnatal carotid body growth (i.e., morphological plasticity), while transient attenuation of carotid body O 2 sensitivity would occur independent of postnatal age. Although the critical period for long‐lasting attenuation of the HVR is limited to the first two postnatal weeks (Bavis et al., J. Appl. Physiol. 92: 1013–1018, 2002), we observed a substantial increase in carotid body volume through 12 wk of age; growth rates and glomus cell division (BrdU labeling) appeared to slow by 8–10 wk of age. In rats exposed to 7 d of 60% O 2 beginning at ~4 wk of age, normoxic ventilation was reduced but HVR was unchanged; normoxic ventilation recovered within 7 d of returning to room air. We conclude that (1) carotid body growth is not the only factor determining the critical period for long‐lasting changes to the HVR and (2) transient changes to the HVR are also limited to exposures during early postnatal development (i.e., prior to P28). Supported by NIH grant P20 RR‐016463 (Maine INBRE).