Submitted on May 11, 2007
Accepted on September 26, 2007
Pulmonary C-fiber receptor activation abolishes uncoupled facial nerve activity from phrenic bursting during positive end-expired pressure in the rat
Kun-Ze Lee1, David D. Fuller2, I-Jung Lu3, Li-Chi Ku4, and Ji-Chuu Hwang1*
1 Life Science, National Taiwan Normal University, Taipei, Taiwan, Taiwan - Republic of China
2 Physical Therapy, University of Florida, Gaineesville, Florida, United States
3 Department of Sports, Health & Leisure, Chihlee Institute of Technology, Taipei, Taiwan, Taiwan - Republic of China
4 National Center for High-performance Computing, Hsinchu Science Park, Hsinchu, Taiwan, Taiwan - Republic of China
* To whom correspondence should be addressed. E-mail: jchwang{at}ntnu.edu.tw.
Phasic respiratory bursting in the facial nerve (FN) can be uncoupled from phrenic bursting by application of positive end-expired pressure (PEEP) at 9 cmH2O. This response reflects excitation of expiratory-inspiratory (EI) and pre-inspiratory (pre-I) facial neurons during the pre-I period and inhibition of EI neurons during inspiration. Because activation of pulmonary C-fiber (PCF) receptors can inhibit the discharge of both EI and pre-I neurons, we hypothesized that PCF receptor activation via capsaicin would attenuate or abolish uncoupled FN bursting during PEEP increased from 3 (baseline) to 9 cmH2O. Neurograms were recorded in the FN and phrenic nerve in anesthetized, ventilated vagally-intact adult Wistar rats. Increasing PEEP to 9 cmH2O resulted in a persistent rhythmic discharge in the FN during periods of phrenic quiescence (i.e. uncoupled bursting). When PEEP was combined with intra-jugular capsaicin injection, uncoupled bursting in the FN was severely attenuated or eliminated (p<0.05). Additional experiments examined the pattern of facial motoneuron (vs. neurogram) bursting during both PEEP and capsaicin. These single fiber recordings confirmed that pre-I and EI neurons (but not I neurons) continued to burst during PEEP-induced phrenic apnea. Application of capsaicin during PEEP substantially inhibited both pre-I and EI neuron discharge. Finally, analyses of FN and motoneuron bursting across the respiratory cycle indicated that the inhibitory effects of capsaicin were more pronounced during the pre-I duration. We conclude that activation of PCF receptors can inhibit FN bursting during PEEP-induced phrenic apnea by inhibiting EI and I facial motoneuron discharge.
