Analysis of slow depolarizing potential in frog taste cell induced by parasympathetic efferent stimulation under hypoxia.
Analysis of slow depolarizing potential in frog taste cell induced by parasympathetic efferent stimulation under hypoxia.
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DOI：
10.1093/chemse/bjm003
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发表时间：
2007-05
期刊：
影响因子：
3.5
通讯作者：
Toshihide Sato;Kazushisa Nishishita;Y. Okada;K. Toda
中科院分区：
文献类型：
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作者：
Toshihide Sato;Kazushisa Nishishita;Y. Okada;K. Toda
强电刺激蛙舌咽（GP）传出神经（ES）可在缺氧条件下引起味觉细胞的慢去极化电位（DP）。本研究旨在阐明慢DPs是否在味觉细胞中被突触后诱导。用筒箭毒碱阻断副交感神经节后，GP神经的ES不能在味细胞中引起慢DPs，因此PSN可引起慢DPs。当缺氧条件下血浆中Ca（2+）浓度降至0.5mM左右时，慢DPs的振幅减小，潜伏期延长。将正常Ca（2+）增加到约20 mM可增加慢DP的幅度并缩短潜伏期。血浆中加入Cd（2+）可使慢DPs的振幅明显降低，潜伏期延长。这些结果表明，慢DPs依赖于味盘突触前PSN末梢的Ca（2+）和Cd（2+）浓度。神经递质P物质神经激肽（1）受体拮抗剂[D-Arg（1），D-Trp（7，9），Leu（11）]-P物质和L-703606完全阻断慢DP。P物质的静脉内应用诱导约7 mV的DP和味觉细胞中约48%的膜电阻降低。一种非选择性阳离子通道拮抗剂氟芬那酸完全阻断慢DP。这些结果表明，慢DP启动突触后在缺氧条件下的青蛙味觉细胞通过打开突触后膜上的非选择性阳离子通道后，P物质可能是从突触前PSN轴突终末释放。
Strong electrical stimulation (ES) of the frog glossopharyngeal (GP) efferent nerve induced slow depolarizing potentials (DPs) in taste cells under hypoxia. This study aimed to elucidate whether the slow DPs were postsynaptically induced in taste cells. After a block of parasympathetic nerve (PSN) ganglia by tubocurarine, ES of GP nerve never induced slow DPs in the taste cells, so slow DPs were induced by PSN. When Ca(2+) in the blood plasma under hypoxia was decreased to approximately 0.5 mM, the slow DPs reduced in amplitude and lengthened in latency. Increasing the normal Ca(2+) to approximately 20 mM increased the amplitude of slow DPs and shortened the latency. Addition of Cd(2+) to the plasma greatly reduced the amplitude of slow DPs and lengthened the latency. These data suggest that the slow DPs depend on Ca(2+) and Cd(2+) concentration at the presynaptic PSN terminals of taste disk. Antagonists, [D-Arg(1), D-Trp(7,9), Leu(11)]-substance P and L-703 606, of neurotransmitter substance P neurokinin(1) receptor completely blocked the slow DPs. Intravenous application of substance P induced a DP of approximately 7 mV and a reduction of membrane resistance of approximately 48% in taste cells. A nonselective cation channel antagonist, flufenamic acid, completely blocked the slow DPs. These findings suggest that the slow DPs are postsynaptically initiated in frog taste cells under hypoxia by opening nonselective cation channels on the postsynaptic membrane after substance P is probably released from the presynaptic PSN axon terminals.