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pubmed-article:1721906pubmed:abstractTextThe bronchus was isolated from actively sensitized guinea pigs, and the effect of antigen challenge on the excitability of bronchial parasympathetic ganglion neurons was examined with standard intracellular recording techniques. Based on histological examination, we found that mast cells were located near parasympathetic ganglia neurons. Antigen challenge resulted in a loss of mast cell staining and the release of the mast cell-associated mediators, histamine (38 ng/g, approximately 14% of total content) and prostaglandin D2 (PGD2, 118 ng/g wet weight of tissue). Challenging the isolated bronchus with the sensitizing antigen resulted in a transient depolarization (mean 6 mV) of the resting membrane potential of the neurons. Antigen challenge also had a dramatic effect on the accommodative properties of the neurons. Before antigen challenge, two subpopulations of neurons could be differentiated by their response to cathodal current steps: 60% of the cells responded in a "phasic" manner, firing one to six spikes and then accommodated, whereas the balance fired spikes repetitively throughout the current pulse. In phasic firing cells, ovalbumin challenge produced a decrease in accommodation. This was evidenced by a fivefold increase in the number of action potentials elicited during a 500-ms suprathreshold current pulse. The antigen-induced depolarization could be mimicked by histamine, whereas the decrease in accommodation was mimicked by application of PGD2. Leukotriene C4, another mast cell-associated mediator, had no effect on these neuronal properties. These results provide evidence that the immediate hypersensitivity response in guinea pig airways may involve changes in membrane characteristics of bronchial parasympathetic ganglia neurons.lld:pubmed
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pubmed-article:1721906pubmed:articleTitleInfluence of antigen on membrane properties of guinea pig bronchial ganglion neurons.lld:pubmed
pubmed-article:1721906pubmed:affiliationDivision of Clinical Immunology, Johns Hopkins Asthma and Allergy Center, Baltimore 21224.lld:pubmed
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