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在离体灌流的牛蛙交感神经节上，氢化可的松一方面通过Ｎ受体介导，快速抑制Ｂ细胞的快兴奋性突触后电位（ｆＥＰＳＰ），引起Ｂ细胞突触传递的阻断。氢化可的松又同时通过Ｍ受体介导，快速增强Ｂ细胞的慢兴奋性突触后电位（ｓＥＰＳＰ），提高Ｂ细胞的兴奋性，使重复放电增加。用阿托品阻断Ｂ细胞上Ｍ受体，可以压抑氢化可的松对ｓＥＰＳＰ的增强效应，增加氢化可的松对Ｂ细胞突触传递的快速抑制作用。
In vitro perfused bullfrog sympathetic ganglia, hydrocortisone, on the one hand, mediates via N-receptors and rapidly inhibits the fast excitatory postsynaptic potential (fEPSP) of B cells, resulting in the blockade of synaptic transmission by B cells. Hydrocortisone, meanwhile, is mediated by M receptor to rapidly increase the slow excitatory postsynaptic potential (sEPSP) of B cells, increase the excitability of B cells and increase the repetitive discharge. Blocking M receptors on B cells with atropine can suppress the enhancement effect of hydrocortisone on sEPSP and increase the rapid inhibitory effect of hydrocortisone on the synaptic transmission of B cells.