The Effects of Caffeine on the Hypercapnic Ventilatory Response

Sudden Infant Death Syndrome (SIDS) is a multifaceted aliment that results in the unexplained death of infants aged one month to one year, with most cases occurring between two to four months. SIDS has also been classified as an ethnic health disparity that affects Native American, and African American infants three to two times more likely, respectively, than Caucasian infants. Caffeine distribution to neonates has shown to significantly reduce the incidence of SIDS via stimulation of the central nervous system by increased alertness and reduced fatigue, however, the mechanism behind caffeine on a neonate’s ability to stimulate breathing is unknown. Central respiratory chemoreceptors are specialized cells that regulate CO2 levels in conjunction with pH levels in the blood. These chemoreceptors are an integral part of the neuronal respiratory circuit that works to monitor and regulate motor output to stimulate breathing. Caffeine is hypothesized to increase sensitivity of central respiratory chemoreceptors, thereby increasing stimulation to minute changes in CO2 levels in the blood. To test the hypothesis that caffeine enhances the CO2 effect on central respiratory chemoreceptors, the animal model of the Lithobates catesbeianus tadpole will be exposed to caffeine chronically for three days. Fictive gill and lung respiratory motor output will be measured using whole nerve recordings of cranial nerve seven (CNVII) and unit field potential firing rates of neurons in chemosensitive areas in the in vitrobrainstem during normocapnic (bath pH 7.8) and hypercapnic (bath pH 7.4) conditions. Partially supported by Ronald E McNair Summer Initiative Grant T217A070291.