BACKGROUND/AIMS: Enteric neuroimmune communication in gastrointestinal hypersensitivity responses includes antigen detection by mast cells and release of chemical messages to the enteric nervous system. The aim of this study was to analyze the electrical and synaptic behavior of neurons in the colonic submucous plexus during exposure to Trichinella spiralis antigen in animals infected earlier with the parasite. METHODS: Microelectrodes were used to record in submucous neurons of guinea pig distal colon during application of Trichinella antigen. RESULTS: Neurons in sensitized animals were more excitable than in controls. Hyperexcitability was seen as a greater probability of spontaneous action potential discharge and repetitive firing to depolarizing current or exposure to acetylcholine. Application of histaminergic antagonists reversed the augmented excitability, suggesting endogenously released histamine as a responsible factor. Antigenic exposure increased neuronal excitability and suppressed nicotinic transmission at fast cholinergic synapses only in sensitized animals. Effects on excitability, but not presynaptic inhibitory effects, were blocked by cimetidine. CONCLUSIONS: Signaling between mucosal mast cells and the enteric nervous system is involved in colonic anaphylactic responses to sensitizing antigens. Histamine is a paracrine signal in the communication pathway.
BACKGROUND/AIMS: Enteric neuroimmune communication in gastrointestinal hypersensitivity responses includes antigen detection by mast cells and release of chemical messages to the enteric nervous system. The aim of this study was to analyze the electrical and synaptic behavior of neurons in the colonic submucous plexus during exposure to Trichinella spiralis antigen in animals infected earlier with the parasite. METHODS: Microelectrodes were used to record in submucous neurons of guinea pig distal colon during application of Trichinella antigen. RESULTS: Neurons in sensitized animals were more excitable than in controls. Hyperexcitability was seen as a greater probability of spontaneous action potential discharge and repetitive firing to depolarizing current or exposure to acetylcholine. Application of histaminergic antagonists reversed the augmented excitability, suggesting endogenously released histamine as a responsible factor. Antigenic exposure increased neuronal excitability and suppressed nicotinic transmission at fast cholinergic synapses only in sensitized animals. Effects on excitability, but not presynaptic inhibitory effects, were blocked by cimetidine. CONCLUSIONS: Signaling between mucosal mast cells and the enteric nervous system is involved in colonic anaphylactic responses to sensitizing antigens. Histamine is a paracrine signal in the communication pathway.
Authors: C U Corvera; O Déry; K McConalogue; P Gamp; M Thoma; B Al-Ani; G H Caughey; M D Hollenberg; N W Bunnett Journal: J Physiol Date: 1999-06-15 Impact factor: 5.182
Authors: David E Reed; Carlos Barajas-Lopez; Graeme Cottrell; Sara Velazquez-Rocha; Olivier Dery; Eileen F Grady; Nigel W Bunnett; Stephen J Vanner Journal: J Physiol Date: 2003-01-24 Impact factor: 5.182