Avenet P, Hofmann F, Lindemann B
Physiology II, Universität des Saarlandes, Homburg, FRG.
Nature. 1988 Jan 28;331(6154):351-4. doi: 10.1038/331351a0.
In taste chemoreception, cyclic adenosine monophosphate (cAMP) appears to be one of the intracellular messengers coupling reception of stimulus to the generation of the response. The recent finding that sweet agents cause a GTP-dependent generation of cAMP poses the question of how this cytosolic messenger acts at the membrane of taste receptor cells. We have shown that cAMP causes a substantial depolarization in these cells. Here we show with whole-cell recordings and inside-out membrane patches that the depolarization caused by cAMP is accounted for by the action of cAMP-dependent protein kinase, which inactivates potassium channels predominantly of 44 pS conductance. Thus, intracellular signalling of the gustatory cells differs from that of olfactory and photoreceptor cells, where cyclic nucleotides control unspecific channels by binding to them rather than by inducing their phosphorylation.
在味觉化学感受中，环磷酸腺苷（cAMP）似乎是将刺激的接收与反应的产生相偶联的细胞内信使之一。最近发现甜味剂会导致cAMP的GTP依赖性生成，这就引发了一个问题：这种胞质信使如何在味觉受体细胞的膜上发挥作用。我们已经表明，cAMP会使这些细胞发生显著的去极化。在此，我们通过全细胞记录和内向外膜片钳实验表明，cAMP引起的去极化是由cAMP依赖性蛋白激酶的作用导致的，该激酶会使主要具有44 pS电导的钾通道失活。因此，味觉细胞的细胞内信号传导不同于嗅觉和光感受器细胞，在嗅觉和光感受器细胞中，环核苷酸通过与非特异性通道结合而非诱导其磷酸化来控制这些通道。
