Skip to main content
. 2016 May 29;595(2):557–570. doi: 10.1113/JP271021

Figure 5. Enteric glia actively regulate gut motility.

Figure 5

Inhibition (A–C) or activation (D–F) of glial calcium (Ca2+) signalling (A and D) results in reduction or stimulation of the gut motor reflex assessed by smooth muscle tension recordings (B and E), respectively, and corresponds to changes in the distal colon motility tested in vivo (C and F). A–C, experiments from tamoxifen‐induced glia‐specific knock out (igKO) of connexin 43 (Cx43) mice (Cx43‐igKO) and the tamoxifen‐treated background strains (Backgr.); figures obtained from McClain et al. (2014). A, neuron‐specific stimulation activates Ca2+ responses in enteric glia and Cx43 is required for the propagation of the glial Ca2+ response (see original work for details). B, electrical field stimulation (EFS) elicits muscle contractions and the contraction force is reduced in the Cx43‐igKO mice. C, selective reduction of the Ca2+ response in the enteric glia reduces distal colon motility in vivo. D–F, experiments from GFAP::hM3Dq transgenic mice, where glial fibrillary acidic protein (GFAP) promoter drives expression of an engineered Gq‐coupled human M3 muscarinic receptor (hM3Dq) and their wild‐type (WT) littermates; figures obtained from McClain et al. (2015). D, enteric glia expressing hM3Dq respond to clozapine N‐oxide (CNO) with an increase in cytosolic Ca2+ and subsequently affect neurally controlled gut reflexes. E, glia‐specific stimulation with CNO evoked response in GFAP::hM3Dq mice similar to stimuli with bethanechol (BCH) and EFS that directly activate smooth muscle and enteric neurons, respectively. Note that CNO effect was blocked by tetrodotoxin (TTX) indicating that glia‐specific effects are mediated via enteric neurons. Also, CNO stimulation evoked no response in WT littermates (see original work). F, selective activation of glial Ca2+ signalling enhances in vivo motility of the distal colon.