Retrotrapezoid nucleus lesions decrease phrenic activity and CO2 sensitivity in rats.

In chloralose-urethane anesthetized, paralyzed, and ventilated rats, we measured the effects of unilateral lesions in the region ventral and ventromedial to the facial nucleus, the retrotrapezoid nucleus (RTN), on eucapnic phrenic activity and the response to increased end-tidal CO2. Chemical (kainic acid injections; 4.7 mM; 10-100 nl) and electrolytic (5-15 mA; 5-15 sec) lesions, anatomically demonstrated to be in the RTN, resulted in a progressive decrease in the amplitude of the integrated phrenic nerve activity from baseline levels of 49-59% of maximum to values of 21-32% of maximum over 30 to 120 min. There were no consistent effects on frequency or on blood pressure. The initial slope of the response to hypercapnia was decreased by 86-92%. Bilateral carotid body ablation did not alter the general pattern of the responses. As in the cat, unilateral RTN lesions decrease baseline phrenic amplitude and virtually abolish the response to hypercapnia. We hypothesize that the RTN region provides; (1) a source of tonic activity which maintains eucapnic ventilatory output, and (2) allows expression of the response to hypercapnia.