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Brainstem control of urethral sphincter relaxation and scent marking behavior

Urination may occur either reflexively in response to a full bladder or deliberately irrespective of immediate need. Voluntary control is desired because it ensures that waste is expelled when consciously desired and socially appropriate1,2. Urine release requires two primary components: bladder pressure and urethral relaxation1–3. Although the bladder contracts during urination, its slow smooth muscle is not under direct voluntary control and its contraction alone is not sufficient for voiding. The decisive action of urination is at the urethral sphincter, where striated muscle permits fast control. This sphincter is normally constricted, but relaxes to enable urine flow. Barrington’s nucleus (Bar, or pontine micturition center) in the brainstem is known to be essential for the switch from urine storage to elimination4–7, and a subset of Bar neurons expressing corticotropin releasing hormone (BarCRH) have recently been shown to promote bladder contraction8–10. However, Bar neurons that relax the urethral sphincter to enable urination behavior have not been identified. Here we describe novel brainstem neurons that control the external urethral sphincter. We find that scent marking behavior in male mice depends upon a subpopulation of spatially clustered Bar neurons that express high levels of estrogen receptor 1 (BarESR1). These neurons are glutamatergic, project to urinary nuclei in the spinal cord with a bias towards sphincter-inhibiting interneurons, and their activity correlates with natural urination. Optogenetic stimulation of BarESR1 neurons rapidly initiates sphincter bursting and efficient voiding in absence of sensory cues in anesthetized and behaving animals. Conversely, inhibiting the activity of these neurons prevents olfactory cues from promoting scent marking behavior. The identification of BarESR1 cells provides an expanded model for the supraspinal control of urination and its dysfunction.