The C1 neurons reside in the rostral ventrolateral medulla (RVLM). They use glutamate as fast transmitter and synthesize catecholamines plus various neuropeptides. Only a third of the C1 neurons are presympathetic i.e. innervate sympathetic preganglionic neurons. These C1 cells include several subgroups that are organized in roughly viscerotopic manner and regulate the circulation in concert with other types of RVLM bulbospinal neurons. Other subsets of C1 cells control the parasympathetic outflow and the hypothalamic pituitary axis including the secretion of vasopressin, oxytocin and corticotrophin releasing factor via direct projections to the dorsal motor nucleus of the vagus and the paraventricular nucleus of the hypothalamus respectively. C1 cells are variously activated by hypoglycemia, infection or inflammation, hypoxia, nociception and hypotension. Optogenetic stimulation of the C1 cells increases breathing and activates brainstem noradrenergic neurons including the locus coeruleus. Based on the various effects attributed to the C1 cells, their axonal projections and what is currently known of their synaptic inputs, we propose that subsets of C1 cells are differentially recruited by pain, hypoxia, infection/ inflammation, hemorrhage and hypoglycemia to produce a repertoire of stereotyped autonomic, metabolic and neuroendocrine responses that help the organism survive physical injury and its associated cohort of acute infection, hypoxia, hypotension and blood loss.