Central respiratory modulation of subretrofacial bulbospinal neurones in the cat.

1. Spontaneous activity was recorded from spinally projecting neurones of the subretrofacial nucleus (s.r.f.) in seven chloralose-anaesthetized, vagotomized, paralysed cats. Nineteen such neurones were identified by their antidromic response to stimulation of the ipsilateral dorsolateral funiculus at C5: their axonal conduction velocities were between 2.1 and 9.1 m/s (mean 5.4), and all were silenced by raising the pressure in the ipsilateral carotid sinus (prepared as a blind sac) to 200 mmHg. DL-homocysteic acid was applied ionophoretically to six of these cells, and these were all excited. 2. Activity was recorded simultaneously from the right phrenic nerve and left cervical sympathetic trunk. The phrenic neurogram was taken as an index of central respiratory drive and used to trigger histograms of s.r.f. neurone activity within the respiratory cycle. To eliminate indirect effects via pressure fluctuations, the remaining arterial baroreceptors were disabled during tests by deflation of the ipsilateral carotid sinus and either section of the contralateral sinus nerve (six cats) or occlusion of the carotid artery (one cat). Phrenic-triggered averages of cervical sympathetic activity were also constructed for comparison. 3. Respiratory modulation was detected in the activity of sixteen out of nineteen s.r.f. neurones. Twelve showed an inspiratory peak in activity that was superimposed on a steady discharge maintained throughout the cycle. Five of this group additionally displayed a post-inspiratory dip in activity to below the late expiratory level, and this feature was also seen in one further cell without any detectable inspiratory peak. Three neurones showed an inverse pattern, with reduced or no activity during inspiration, followed by a 'rebound' increased activity level during the post-inspiratory period. The remaining three cells had no discernible respiratory rhythm. 4. Raising end-tidal CO2 levels increased the degree of respiratory modulation in all six inspiratory-firing cells tested as well as one cell showing inspiratory inhibition. Within the range tested, CO2 had no clear effect on the respiratory modulation of two other cells showing inspiratory inhibition and one showing only post-inspiratory depression. No consistent relation was apparent between the overall firing rate of neurones and end-tidal CO2. 5. These results are discussed with reference to the respiratory modulation of sympathetic neurone activity. It is suggested that s.r.f. neurones supply respiratory-related as well as tonic drive to preganglionic neurones.