CHEMOAFFERENT DEGENERATION AND CAROTID-BODY HYPOPLASIA FOLLOWING CHRONIC HYPEROXIA IN NEWBORN RATS

1. To define the role of environmental oxygen in regulating postnatal maturation of the carotid body afferent pathway, light and electron mi croscopic methods were used to compare chemoafferent neurone survival and carotid body development in newborn rats reared from birth in norm oxia (21 % O-2) or chronic hyperoxia (60 % O-2). 2. Four weeks of chro nic hyperoxia resulted in a significant 41% decrease in the number of unmyelinated axons in the carotid sinus nerve, compared with age-match ed normoxic controls. In contrast, the number of myelinated axons was unaffected by hyperoxic exposure. 3. Chemoafferent neurones, located i n the glossopharyngeal petrosal ganglion, already exhibited degenerati ve changes following 1 week of hyperoxia from birth, indicating that e ven a relatively short hyperoxic exposure was sufficient to derange no rmal chemoafferent development. In contrast, no such changes were obse rved in the vagal nodose ganglion, demonstrating that the effect of hi gh oxygen levels was specific to sensory neurones in the carotid body afferent pathway. Moreover, petrosal ganglion neurones were sensitive to hyperoxic exposure only during the early postnatal period. 4. Chemo afferent degeneration in chronically hyperoxic animals was accompanied by marked hypoplasia of the carotid body. In view of previous finding s from our laboratory that chemoafferent neurones require trophic supp ort from the carotid body for survival after birth, we propose that ch emoafferent degeneration following chronic hyperoxia is due specifical ly to the loss of target tissue in the carotid body.