Effects of unilateral lesions of retrotrapezoid nucleus on breathing in awake rats

Akilesh, Manjapra R., Matthew Kamper, Aihua Li, and EugeneE. Nattie. Effects of unilateral lesions of retrotrapezoid nucleuson breathing in awake rats. J. Appl.Physiol. 82(2): 469-479, 1997.In anesthetizedrats, unilateral retrotrapezoid nucleus (RTN) lesions markedlydecreased baseline phrenic activity and the response toCO₂ (E. E. Nattie and A. Li.Respir. Physiol. 97: 63-77,1994). Here we evaluate the effects of such lesions on restingbreathing and on the response to hypercapnia and hypoxia inunanesthetized awake rats. We made unilateral injections 24 ± 7 (SE) nl] of ibotenic acid (IA; 50 mM), an excitatoryamino acid neurotoxin, in the RTN region(n = 7) located by stereotaxic coordinates and by field potentials induced by facial nervestimulation. Controls (n = 6) receivedRTN injections (80 ± 30 nl) of mock cerebrospinal fluid. A secondcontrol consisted of four animals with IA injections (24 ± 12 nl)outside the RTN region. Injected fluorescent beads allowed anatomicidentification of lesion location. Using whole body plethysmography, wemeasured ventilation in the awake state during room air, 7%CO₂ in air, and 10%O₂ breathing before and for 3 wkafter the RTN injections. There was no statistically significant effectof the IA injections on resting room air breathing in the lesion groupcompared with the control groups. We observed no apnea. The response to7% CO₂ in the lesion groupcompared with the control groups was significantly decreased, by 39%on average, for the final portion of the 3-wk study period. There wasno lesion effect on the ventilatory response to 10%O₂. In this unanesthetized model,other areas suppressed by anesthesia, e.g., the reticular activatingsystem, hypothalamus, and perhaps the contralateral RTN, may providetonic input to the respiratory centers that counters the loss of RTNactivity.