Sexual dysfunction is a common complication in men with chronic spinal cord injury. In particular, ejaculation is severely compromised or absent and the resulting infertility issues are important to this group of predominantly young men. To investigate the neural circuits and descending spinal pathways involved in ejaculation, animal models have been developed in normal and spinal cord-injured preparations. Primarily through studies in rats, spinal ejaculatory circuits have been described including (i) autonomic circuits at the thoracolumbar and lumbosacral levels mediating the emission phase of ejaculation, (ii) somatic circuits at the lumbosacral level controlling the expulsion phase of ejaculation through sequential and rhythmic contraction of perineal striated muscles (e.g. bulbospongiosus), and (iii) a proposed ejaculatory pattern generator in the lumbar cord. Midthoracic incomplete chronic spinal cord injury has revealed the dependency of spinal ejaculatory circuits on bilateral spinal pathways from the brainstem via modulation of pudendal motor neuron reflexes and pudendal nerve autonomic fibers. Accordingly, sensory input from the dorsal nerve of the penis, required to trigger the ejaculatory response in animals and humans, is no longer inhibited from the lateral paragigantocellularis nucleus in the ventrolateral medulla. This inhibitory effect, likely presynaptic through a serotonergic pathway, is thought to be necessary to provide the rhythmic, bursting, and sequential contractions of the perineal muscles during ejaculation. Chronic lateral hemisection injury, which severs half of the descending lateral funiculus-located pathways, results in new functional connections of the pudendal reflex inhibitory and pudendal sympathetic activation pathways across the midline, above and below the lesion, respectively. Clinical correlations in spinal cord-injured men have demonstrated the validity of the rodent animal for the study of ejaculatory dysfunction after chronic injury.