Figure 12.

A schematic diagram illustrates the reestablished vasomotor pathways. Primary afferent fibers initiating from arterial chemoreceptors and baroreceptors project excitatory inputs to the NTS in the brainstem. Parasympathetic baroreceptor afferent fibers ascend in the vagus and glossopharyngeal cranial nerves, providing inhibitory inputs to the NTS. As a major recipient of primary sensory cardiovascular information, the NTS precisely regulates hemodynamic performance through the caudal ventrolateral medulla (CVLM) and the RVLM. At the brainstem level, neurons in the RVLM and other presympathetic nuclei originate supraspinal vasomotor fibers projecting to the SPNs in the IML of spinal cord, regulating cardiovascular function. High-level SCI often interrupts this descending control and results in disordered hemodynamics. Transplanting embryonic RN-NSCs into the lesion extends projections onto the SPNs in the caudal spinal cord. On the other hand, the cellular graft facilitates the regeneration of disrupted host supraspinal vasomotor pathways and forms synapses with grafted neurons. Thus, supraspinal autonomic pathways are rebuilt via a relay-based indirect circuit to regulate cardiovascular function following SCI.