Intercostal and abdominal muscle afferent influence on pneumotaxic center respiratory neurons.

The experiments were performed on mid-collicular decerebrated, vagotomized, paralyzed, artificially ventilated cats. Phrenic (PA) and pneumotaxic center (PC) respiratory neuron (extracellular) activities were recorded during electrical stimulation of intercostal nerve proprioceptor afferents (external, internal or lateral intercostal nerves). Intercostal nerve stimulation (INS) of sufficient intensity to reduce PA also reduced the activity of phasic PC I-neurons and the I-modulated portion of tonic firing I-neurons. The stimulus-response latency for the reduction in PA was always shorter than the latency for the reduction in I-neuron activity. Baseline tonic activity (during E-phase) was unaffected by INS in most tonic I-neurons. The predominant response of PC IE- and E-neurons to INS was augmentation of their activity. Stimulus-response latency studies showed that the increase in IE- and E-neuron activity occurred after the decrease in PA. It is concluded that: (1) the reduced PC I-neuron activity following INS is due primarily to disfacilitation resulting probably from decreased activity in medullary I-neurons that drive the PC I-neurons, (2) PC IE- and E-neurons are not the primary neurons mediating the inspiratory inhibitory effects of intercostal and abdominal muscle proprioceptors on medullary I drive, (3) the changes in PC IE- and E-neuron activity is not due secondarily to changes in DRG and VRG IE- or E-neuron activities, and (4) the reflex effects are due to stimulation of low threshold Group I afferent fibers.