Geran Laura C, Spector Alan C
Department of Psychology and Center for Smell and Taste, University of Florida, Gainesville, FL 32611-2250, USA.
Behav Neurosci. 2004 Feb;118(1):178-83. doi: 10.1037/0735-7044.118.1.178.
Amiloride-insensitive sodium taste transduction is severely limited by large anions (i.e., gluconate). We found that in a brief-access taste test, sodium-depleted rats exhibited similar levels of increased licking to several sodium salts regardless of anion but did not increase licking to nonsodium salts compared with water. The enhanced licking of sodium salts was abolished in the presence of amiloride. These results suggest that the amiloride-sensitive taste transduction pathway is not only necessary but that it is also sufficient for sodium identification in rats. Sodium-depleted rats tested with amiloride initiated significantly more trials than nondepleted rats; hence, appetitive behavior was mildly potentiated by depletion, even in the absence of a sodium taste cue. Overall, these findings provide compelling support for the primacy of the amiloride-sensitive taste transduction mechanism and its associated neural pathway in the recognition of the sodium cation.
对氨氯吡咪不敏感的钠味觉转导受到大阴离子（即葡萄糖酸盐）的严重限制。我们发现，在一个短暂接触的味觉测试中，缺钠大鼠对几种钠盐表现出相似程度的舔舐增加，而不论阴离子如何，但与水相比，对非钠盐并未增加舔舐。在氨氯吡咪存在的情况下，对钠盐的增强舔舐被消除。这些结果表明，对氨氯吡咪敏感的味觉转导途径不仅是必要的，而且对于大鼠识别钠也是充分的。用氨氯吡咪测试的缺钠大鼠比未缺钠大鼠发起的试验显著更多；因此，即使在没有钠味觉线索的情况下，食欲行为也因缺钠而略有增强。总体而言，这些发现为对氨氯吡咪敏感的味觉转导机制及其相关神经通路在识别钠阳离子中的首要地位提供了有力支持。
