Reticulospinal vasomotor neurons of the rat rostral ventrolateral medulla: relationship to sympathetic nerve activity and the C1 adrenergic cell group.
Academic Article
Overview
abstract
Neurons projecting from the rostral ventrolateral medulla (RVL) to the spinal cord were antidromically identified in rats anesthetized with urethane, paralyzed, and ventilated. The sites of lowest antidromic threshold were concentrated in the intermediolateral nucleus (IML). Their axonal conduction velocities were distributed bimodally, with the mean of the rapidly conducting fibers (greater than 1 m/sec) being 3.1 +/- 0.1 m/sec (n = 105), and of the slower axons being 0.8 +/- 0.03 m/sec (n = 25). Single-shock electrical stimulation of RVL elicited 2 bursts of excitation in splanchnic sympathetic nerve activity (SNA), which resulted from activation of 2 descending pathways with conduction velocities comparable to those of antidromically excited RVL-spinal neurons. The probability of discharge of RVL-spinal cells was synchronized both with the cardiac-related bursts in SNA with functional baroreceptor reflexes and with the free-running 2-6 Hz bursts in SNA following baroreceptor afferent denervation. On the average, their spontaneous discharges occurred 67 +/- 2 msec (n = 31) prior to the peak of the spontaneous bursts in splanchnic SNA. This time corresponded to the latency to the peak of the early excitatory potential in splanchnic SNA following electrical stimulation of RVL. Baroreceptor reflex activation inhibited RVL-spinal neurons. The recording sites of RVL-spinal vasomotor neurons were consistently located within 100 micron of cell bodies (C1 neurons) immunoreactive for the adrenaline-synthesizing enzyme phenylethanolamine N-methyltransferase (PNMT). Ultrastructural analysis of the lateral funiculus of the cervical and thoracic spinal cord demonstrated PNMT immunoreactivity within myelinated (0.6-2.1 micron diameter) and unmyelinated (0.1-0.8 micron diameter) axons. Estimated conduction velocities of these fibers were comparable to the antidromic conduction velocities of the rapidly and slowly conducting populations of RVL-spinal vasomotor neurons. We conclude that in rat, the discharge of RVL-spinal vasomotor neurons strongly influences SNA: the baroreceptor-mediated inhibition of these neurons is reflected in the cardiac locking of SNA, while, in the absence of baroreceptor input, the synchronous discharge of RVL-spinal neurons maintains a free-running 2-6 Hz bursting pattern in SNA. RVL-spinal neurons are located within, and may be elements of, the C1 adrenergic cell group, and they provide a sympathoexcitatory drive to neurons in the IML over rapidly and slowly conducting pathways that correspond to myelinated and unmyelinated spinal axons containing PNMT.
