Neonatal rats exhibit a critical period of vulnerability to sustained hypoxia between 11 and 15 days of age. Specifically, these pups exhibit blunted hypoxic ventilatory responses (HVR) and increased mortality in subsequent days which is not observed in normoxia-reared controls or in pups exposed to sustained hypoxia at earlier or later ages (Mayer et al., J Appl Physiol 116: 514-521, 2014). To determine whether carotid body dysfunction contributes to these phenotypes, Lewis rat pups were exposed to sustained hypoxia (10.2% O 2 ) or normoxia (20.9% O 2 ) from P11 to P15 (SH11-15 and NX11-15, respectively). On the following day (P16), we assessed carotid body function by recording single-unit carotid chemoafferent activity from the petrosal ganglion in vitro. Preliminary experiments suggested that SH11-15 pups overexpress components of the extracellular matrix (ECM) in the carotid body, so some preparations were incubated in either hyaluronidase (8 U/ml) or chondroitinase ABC (ChABC; 0.1 U/ml) for 30 minutes to partially digest the ECM prior to electrophysiological recordings. Baseline chemoafferent activity was similar across treatment groups. However, peak discharge frequency in hypoxia (5% O 2 ) was significantly reduced in the SH11-15 group (6.9±0.8 vs. 12.6±1.3 imp/s (mean±SEM); P=0.001). Enzyme treatments did not rescue carotid body function in the SH11-15 group; instead, ChABC actually reduced hypoxic chemoafferent activity in the NX11-15 group (4.8±1.1 imp/s; P< 0.001 vs. no enzyme). Collectively, these data suggest that reduced carotid body O 2 sensitivity contributes to the blunted HVR previously reported in SH11-15 rat pups. Although acute digestion of the ECM did not rescue carotid body O 2 sensitivity, chronic changes in ECM could still contribute to abnormal carotid body development. These data may have implications for our understanding of carotid body abnormalities and respiratory control dysfunction in sudden infant death syndrome (SIDS). Supported by NIH grants R01 HD111415 and P20 GM103423. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Bavis et al. (Fri,) studied this question.