Hydrogen sulfide as a signaling molecule in the enteric nervous system

P>Hydrogen sulfide (H2S) is produced by sulfate-reducing bacteria present in the colon. Recently, it has been demonstrated that mammals have enzymatic pathways to produce H2S. As H2S was added to the list of gaseous signaling molecules, the number of papers related to H2S biology has increased exponentially. However, the physiological role of H2S in the gastrointestinal tract is still unknown. Endogenous production in different cell types indicates that H2S might participate in various functions such as pain, motility and secretion. Nevertheless, experimental protocols to demonstrate a physiological role for H2S are not easy to perform due to the lack of specific antagonists. Genetically modified animals lacking a specific route of H2S synthesis are useful biological tools although whether they alter gastrointestinal function are still unknown. In this issue of Neurogastroenterology and Motility, Krueger et al. examine the role of H2S in secretion and in afferent neuronal activation using sodium hydrosulfide as a source of H2S. Interestingly, sodium hydrosulfide causes secretion and increased spike activity in afferent neurons. The mechanism partly involves transient receptor potential vanilloid type I located on afferent neurons, causing local release of substance P, which in turn activates cholinergic secretomotor neurons. These novel observations extend our understanding of the function of H2S in the gastrointestinal tract.