During embryonic and postnatal development, the neurons that control the respiratory function go through a process of "maturation". In this process, these neurons acquire a precise communication network that allows them to generate a robust ventilatory rhythm that is adjustable to the physiological needs of the body. A dysfunction or an abnormal development of these neurons can lead to a variety of important respiratory disorders. Indeed, babies born prematurely (with an immature neural respiratory network) have a higher risk of developing respiratory irregularities.
These irregularities are manifested in form of repeated respiratory arrests (apnea of prematurity - AoP) that induce blood deoxygenation, which in clinical terms are called intermittent hypoxia (IH). IH, in turn, delays the maturation and development of the respiratory neural system, increases morbidity, prolongs the need for hospitalization care, and has long-term cognitive and neurological outcomes. Since mitochondria are tiny structures inside the cell that use oxygen to produce all the energy required by the brain, this research program proposes to study how IH affects the functioning of brain mitochondria at neonatal ages.
To do so, we will use rats pups exposed to IH (a classical model to study AoP in the laboratory). Likewise, we plan to investigate whether new mitochondrial-target drugs, currently used to prevent mitochondrial dysfunction, could be used to ameliorate the damage caused by the IH associated with AoP. In addition, since: 1) neonatal respiratory diseases are more common in men than in women, and 2) sex steroid hormones modulate the mitochondrial functioning, we plan to characterize the impact of IH in the mitochondria of both sexes. Thus, our research will lead to the identification of new, more effective, and sex-tailored treatments.