Cardiac Responses to Carbon Dioxide in Developing Zebrafish (Danio rerio)

Abstract

The ontogeny of carbon dioxide (CO2) sensing in zebrafish (Danio rerio) has not been studied. In this thesis, CO2-mediated increases in heart rate were used to gauge the capacity of zebrafish larvae to sense CO2. CO2 is thought to be sensed through neuroepithelial cells (NECs), which are homologous to mammalian carotid body glomus cells. Owing to its role in facilitating intracellular acidification during exposure to hypercapnia, it was hypothesized that carbonic anhydrase (CA) is involved in CO2 sensing, and that inhibition of CA would blunt the downstream responses. The cardiac response to hypercapnia (0.75% CO2) was reduced in fish exposed to acetazolamide, a CA inhibitor, and in fish experiencing CA knockdown. Based on pharmacological evidence using β-adrenergic receptor (ß-AR) antagonists, and confirmed by β1AR gene knockdown, the efferent limb of the reflex tachycardia accompanying hypercapnia is probably mediated by sympathetic adrenergic neurons interacting with cardiac β1 receptors.