Axonal branching patterns and funicular trajectories of raphespinal sympathoinhibitory neurons

We studied axonal branching patterns and funicular trajectories of cat medullary raphespinal neurons with spontaneous activity related to inferior cardiac postganglionic sympathetic nerve discharge (as demonstrated with spike-triggered averaging). These neurons were excited by raising carotid sinus pressure. We have classified these neurons as sympathoinhibitory in function and refer to them here as RS neurons. Microstimulation of the second thoracic spinal segment (T2) antidromically activated RS neurons (as determined with time-controlled collision of spontaneous and evoked action potentials). The longest-latency antidromic responses were elicited with the lowest-threshold current from sites in the intermediolateral nucleus (IML). This observation suggests that RS neurons innervated IML. Most RS neurons activated from T2 were also antidromically activated by stimulation of a more caudal thoracic spinal segment (T6 or T12). Time-controlled collision of action potentials evoked by stimulation at two thoracic levels allowed us to distinguish activation of an axonal branch in T2 from that of the main axon coursing through T2 to the more caudal thoracic level. Of those RS axons that branched in T2, 78% descended at least as far caudal as T6, whereas 65% reached T12. The axonal projections of other RS neurons that innervated T2 were restricted to no more than two consecutive thoracic spinal segments (as determined by stimulation in T3). Antidromic mapping of T2 further revealed that the axons of RS neurons coursed through the dorsolateral, ventral, or ventrolateral funiculus to innervate the ipsilateral and/or contralateral IML. The conduction velocities of dorsolateral and ventral RS axons indicated that they were finely myelinated. The data demonstrate the existence of RS neurons with restricted and widespread axonal branching patterns, thereby supporting the view that the medullary raphe complex is capable of regional as well as global inhibitory control over spinal sympathetic outflow.