Is Mitochondrial Development Impaired in Hyperoxic Rats and does this Underpin the Blunting of the Acute Hypoxic Ventilatory Response?

Carotid body (CB) responses to hypoxia are low at birth and increase over time to mature responses. Using an in vitro rat CB-carotid sinus nerve (CSN) preparation, Kholwadwala and Donnelly (1992) demonstrated that the CSN activity in response to hypoxia increased from low levels to robust adult responses after two weeks. This time course of maturation was paralleled by an increase in TASK channel sensitivity to hypoxia in the O2-sensing Type I cells (Kim et al, 2011). Previous studies have indicated that a fall in Type I cell mitochondrial volume and an increase in the rate of oxidative phosphorylation may underpin the development of the hypoxic ventilatory response (Paulet et al, 2012). Previously, the lab has seen a significant reduction in mitochondrial volume during development in normoxic reared rats. Our most recent studies addressed the phenomenon that hyperoxia delays the maturation of the acute hypoxic response (Bavis, RW et al, 2010) and that this may be via an effect on type I cell mitochondria. However, contrary to Paulet et al, our findings demonstrated that in control conditions mitochondrial volume did not fall during development. This made interpretations of the hyperoxia experiments impossible