title: Lactobacillus reuteri enhances excitability of colonic AH neurons by inhibiting calcium-dependent potassium channel opening.
abstract: Probiotics are live non-pathogenic commensal organisms that exert therapeutic effects in travellers' diarrhea, irritable bowel syndrome and inflammatory bowel disease. Little is known about mechanisms of action of commensal bacteria on intestinal motility and motility-induced pain. It has been proposed that probiotics affect intestinal nerve function, but direct evidence for this has thus far been lacking. We hypothesized that probiotic effects might be mediated by actions on colonic intrinsic sensory neurons. We first determined whether sensory neurons were present in rat colon by their responses to chemical mucosal stimulation and identified them in terms of physiological phenotype and soma morphotype. Enteric neuron excitability and ion channel activity were measured using patch clamp recordings. We fed 10(9)Lactobacillus reuteri (LR) or vehicle control to rats for 9 days. LR ingestion increased excitability (threshold for evoking action potentials) and number of action potentials per depolarizing pulse, decreased calcium-dependent potassium channel (IK(Ca)) opening and decreased the slow afterhyperpolarization (sAHP) in sensory AH neurons, similar to the IK(Ca) antagonists Tram-34 and clotrimazole. LR did not affect threshold for action potential generation in S neurons. Our results demonstrate that LR targets an ion channel in enteric sensory nerves through which LR may affect gut motility and pain perception.
authors.affiliation: The Brain-Body Institute, St. Joseph's Healthcare, Hamilton, ON, Canada.|Department of Psychiatry and Behavioral Neurosciences, McMaster University, Hamilton, ON, Canada.
authors.forename: Wolfgang A
authors.initials: WA
authors.lastname: Kunze
authors.affiliation: The Brain-Body Institute, St. Joseph's Healthcare, Hamilton, ON, Canada.
authors.forename: Yu-Kang
authors.initials: YK
authors.lastname: Mao
authors.affiliation: Department of Medicine, McMaster University, Hamilton, ON, Canada.
authors.forename: Bingxian
authors.initials: B
authors.lastname: Wang
authors.affiliation: Department of Medicine, McMaster University, Hamilton, ON, Canada.
authors.forename: Jan D
authors.initials: JD
authors.lastname: Huizinga
authors.affiliation: The Brain-Body Institute, St. Joseph's Healthcare, Hamilton, ON, Canada.
authors.forename: Xuelian
authors.initials: X
authors.lastname: Ma
authors.affiliation: The Brain-Body Institute, St. Joseph's Healthcare, Hamilton, ON, Canada.|Department of Medicine, McMaster University, Hamilton, ON, Canada.
authors.forename: Paul
authors.initials: P
authors.lastname: Forsythe
authors.affiliation: The Brain-Body Institute, St. Joseph's Healthcare, Hamilton, ON, Canada.|Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada.
authors.forename: John
authors.initials: J
authors.lastname: Bienenstock
mesh_terms: D000818:Animals; D003106:Colon / Q000166:cytology / Q000502:physiology*; D015640:Ion Channel Gating / Q000502:physiology*; D052200:Limosilactobacillus reuteri / Q000502:physiology*; D008297:Male; D009474:Neurons / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology*; D024681:Potassium Channels, Calcium-Activated / Q000037:antagonists & inhibitors* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D015221:Potassium Channels; D024681:Potassium Channels, Calcium-Activated