Whole Nerve Recordings and Extracellular Field Potentials of Central Respiratory Chemoreceptive Areas in Response to Normocapnic and Hypercapnic Conditions

Sudden Infant Death Syndrome (SIDS) is the leading cause of death in postneonatal infants one month to one year of age. Programs with the goal of reducing incidence of SIDS have been successful, though the cause of SIDS is still unknown. In this lab, an in vitro larval Lithobates catesbeianus brainstem preparation is used, allowing for manipulation while maintaining an intact respiratory circuit for extended amounts of time. Experiments were designed in order to test the hypothesis that a failure in CO₂ chemoreception in the brain prevents infants from increasing respiratory rate when in hypercapnic conditions. Fictive gill and lung patterns will be monitored in the Lithobates catesbeianus tadpole using whole nerve recordings at cranial nerve (CN) VII. The firing rates of neurons in a central respiratory chemoreceptive area will be monitored via their extracellular field potentials. The photosensitive dye BCECF will be used to determine the intracellular pH (pHi) of the neuron. Experimental conditions will be at normocapnic (bath pH= 7.8) levels, with the brainstem preparation later exposed to hypercapnic (7.4) conditions. We expect that in hypercapnic bath conditions, the neurons will fire action potentials at a much higher rate. In hypercapnic conditions, the firing of action potentials is expected to be directly proportional to motor output and inversely proportional to the pHi of the neuron.  By studying the respiratory motor output of tadpoles, the underlying mechanisms of SIDS could be investigated. Partially supported by TWD MARC GM07717.