Abstract:
This research investigated location of the lung respiratory rhythm generator (RRG) in the bullfrog brainstem using neurokinin-1 (NK1R) and [mu]opioid ([mu]OR) receptor colocalization and characterized the role of these receptors in breathing pattern formation. colocalization was distinct near the facial nucleus in juvenile bullfrogs but not in tadpoles. NK1R intensity exhibited no developmental change, while [mu]OR intensity increased from late-stage tadpoles to juvenile frogs. Substance P (NK1R agonist; bath applied) increased lung burst frequency, lung burst cycle frequency (BCF), episode frequency, lung burst amplitude and area, but decreased number of lung bursts per episode and lung burst duration. Antagonist D decreased lung burst frequency and BCF, episode frequency, and the number of lung bursts per episode, and increased lung burst duration and area. DAMGO ([mu]OR agonist; bath applied) decreased lung burst frequency and BCF, episode frequency, and number of lung bursts per episode, but increased all lung burst parameters. Naloxone ([mu]OR antagonist) increased lung burst frequency and BCF, episode frequency, lung bursts per episode but decreased all lung burst parameters. Together these results indicate that NK1R and [mu]OR colocalization represents the lung RRG, and that episode formation is intrinsic to the respiratory control network but may or may not originate in the RRG.
