Functional alterations in gut contractility after connexin36 ablation and evidence for gap junctions forming electrical synapses between nitrergic enteric neurons

•Cx36 forms gap junctions between enteric neurons that express nitric oxide synthase.•Spontaneous and stimulus-induced gut contractions are altered in Cx36 knockout mice.•Impairments in the ko mice suggest deficits in enteric inhibitory neurons.•Dysfunction of enteric neuronal gap junctions may exacerbate human gut disorders. Neurons in the enteric nervous system utilize numerous neurotransmitters to orchestrate rhythmic gut smooth muscle contractions. We examined whether electrical synapses formed by gap junctions containing connexin36 also contribute to communication between enteric neurons in mouse colon. Spontaneous contractility properties and responses to electrical field stimulation and cholinergic agonist were altered in gut from connexin36 knockout vs. wild-type mice. Immunofluorescence revealed punctate labelling of connexin36 that was localized at appositions between somata of enteric neurons immunopositive for the enzyme nitric oxide synthase. There is indication for a possible functional role of gap junctions between inhibitory nitrergic enteric neurons.