Synaptic response of bulbar respiratory neurons to hypercapnic stimulation in peripherally chemodenervated cats.

Effects of hypercapnia on the membrane potential and synaptic activity of bulbar respiratory neurons were studied in decerebrate, vagotomized, glomectomized and artificially ventilated cats. Coaxial multibarrelled electrodes were used for intracellular recording and extracellular iontophoresis of drugs. Hypoventilation with oxygen-enriched air (hyperoxic hypercapnia) produced an increase of depolarization together with an increase of spiking during the active phase and an increase of hyperpolarization during the inactive phase of each respiratory cycle in the inspiratory, postinspiratory and expiratory neurons of the ventral respiratory group. Both depolarizing and hyperpolarizing effects were associated with a decrease in input resistance. Intracellular injection of Cl- reversed the polarity of the hyperpolarizing synaptic wave to depolarization during the inactive phase, and hypercapnia increased the depolarization at that phase. Iontophoresis of tetrodotoxin eliminated the CO2-induced changes in membrane potential and input resistance. In 20 out of 58 neurons examined, iontophoretically applied atropine partly or totally suppressed the depolarizing response to hypercapnia. For these neurons, iontophoresed acetylcholine produced a sustained depolarization that was antagonized by atropine, but not by hexamethonium. The present study shows that both depolarizing and hyperpolarizing responses of medullary respiratory neurons to hyperoxic hypercapnia are synaptically mediated. A muscarinic mechanism is involved in part of the respiratory neuronal excitation evoked by hypercapnia.