Weinreich D, Undem B J
J Clin Invest. 1987 May;79(5):1529-32. doi: 10.1172/JCI112984.
We have attempted to identify a role for mast cells in autonomic ganglia by examining the effects of antigen challenge on mast cell-associated mediator release and synaptic transmission through the superior cervical ganglion isolated from ovalbumin-sensitized guinea pigs. Ovalbumin induced the release of 7.9 ng of histamine, 40 pg of immunoreactive sulfidopeptide-leukotriene, and 140 pg of immunoreactive-PgD2 per ganglion. Ovalbumin produced long-lasting potentiation (51 +/- 4%, mean +/- SEM, n = 66) of synaptic transmission, the protracted nature of which could not be mimicked by exogenous histamine (10(-5) M). Selective histamine H1 antagonists inhibited the antigen-induced potentiation, but did not reverse it when added any time after antigen exposure. These results indicate that immunologic activation of mast cells can directly potentiate neurotransmission in sympathetic ganglia. Histamine appears to be a mediator involved in the induction of antigen-induced potentiation of synaptic transmission, but alone cannot account for the long term nature of this phenomenon.
我们试图通过检查抗原激发对肥大细胞相关介质释放以及通过从卵清蛋白致敏豚鼠分离的颈上神经节的突触传递的影响,来确定肥大细胞在自主神经节中的作用。卵清蛋白诱导每个神经节释放7.9 ng组胺、40 pg免疫反应性硫化肽白三烯和140 pg免疫反应性PgD2。卵清蛋白使突触传递产生持久增强(51±4%,平均值±标准误,n = 66),其持续性质无法被外源性组胺(10⁻⁵ M)模拟。选择性组胺H1拮抗剂抑制抗原诱导的增强作用,但在抗原暴露后任何时间添加均不能使其逆转。这些结果表明肥大细胞的免疫激活可直接增强交感神经节中的神经传递。组胺似乎是参与诱导抗原诱导的突触传递增强的介质,但单独不能解释该现象的长期性质。