Premium
Bifidobacterium longum NCC 3001 inhibits AH neuron excitability
Author(s) -
Khoshdel A.,
Verdu E. F.,
Kunze W.,
McLean P.,
Bergonzelli G.,
Huizinga J. D.
Publication year - 2013
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/nmo.12147
Subject(s) - bifidobacterium longum , hyperpolarization (physics) , depolarization , patch clamp , chemistry , neuroscience , sensory system , potassium channel , electrophysiology , neuron , biology , endocrinology , bifidobacterium , biochemistry , organic chemistry , nuclear magnetic resonance spectroscopy , fermentation , lactobacillus
Background B ifidobacterium longum (B. longum) NCC 3001 can affect behavior and brain biochemistry, but identification of the cellular targets needs further investigation. Our hypothesis was that the communication with the brain might start with action on enteric sensory neurons. Methods Ileal segments from adult mice were used to create a longitudinal muscle‐myenteric‐plexus preparation to expose sensory after‐hyperpolarizing ( AH ) neurons in the myenteric plexus to allow access with microelectrodes. The intrinsic excitability of AH neurons was tested in response to the perfusion of conditioned media (B. longum culture supernatant) or unconditioned media (growth medium, MRS ). Key Results B. longum conditioned medium significantly reduced the excitability of AH neurons compared to perfusion with the unconditioned medium. Specifically, a reduction was seen in the number of action potentials fired per depolarizing test pulse, the instantaneous and time‐dependent input resistances and the magnitude of the hyperpolarization‐activated cationic current (I h ). Conclusions & Inferences The probiotic B . longum reduces excitability of AH sensory neurons likely via opening of potassium channels and closing of hyperpolarization‐activated cation channels.