Figure 2. Effect of hypercapnia on the discharge rate of putative bulbospinal vasomotor neurons of the rostral ventrolateral medulla (RVLM) in vagotomized and sino-aortic deafferented rats.

A, effect produced by stepping end-expiratory CO₂ from 5 to 10% on the discharge of a putative bulbospinal vasomotor neuron. B, time-controlled collision test showing that the neuron shown in A sends an axon to or through spinal segment T3 (* indicates two sweeps when collision occurred. Collisions (absence of the antidromic spike, a, were caused by decreasing the interval between a spontaneous spike, s, and the stimulus delivered to the spinal cord (arrow). C, procedure used to label the cell juxtacellularly with biotinamide (upper trace: unit; lower trace current monitor; 3.4 nA). D, mean effect of stepping CO₂ from 5 to 10% on 11 bulbospinal RVLM neurons (*P < 0.05 from both control and recovery values). E, location of the biotinamide-labelled neurons. The two coronal sections represent from top to bottom Bregma −11.6 and −11.8 mm after Paxinos & Watson (1998). F, PND-triggered activity histogram of the RVLM bulbospinal neuron shown in A–C reveals a respiratory pattern reminiscent of that of the splanchnic nerve. G, different RVLM neuron exhibiting a respiratory pattern reminiscent of that of the lumbar nerve. Amb, ambiguus nucleus; IO, inferior olive; py, pyramidal tract; RPa, raphe pallidus; sp5, spinal tract of trigeminal nerve; VII, facial motor nucleus.