Attenuation of peripheral salt taste responses and local immune function contralateral to gustatory nerve injury: effects of aldosterone
Attenuation of peripheral salt taste responses and local immune function contralateral to gustatory nerve injury: effects of aldosterone
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DOI：
10.1152/ajpregu.00219.2009
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发表时间：
2009-10-01
影响因子：
2.8
通讯作者：
Hill, David L.
中科院分区：
文献类型：
--
作者：
Guagliardo, Nick A.;West, Katie Nicole;Hill, David L.
Guagliardo NA，West KN，McClubkey LP，Hill DL.味觉神经损伤对侧外周盐味觉反应和局部免疫功能的减弱：醛固酮的影响。Am J Physiol Regul Integr Comp Physiol 297：R1103-R1110，2009.首次发表于2009年8月12日; doi：10.1152/ajpregu.00219.2009。饮食钠限制再加上轴突切断大鼠鼓索神经（CTX）的结果选择性衰减味觉反应的钠盐在对侧，完整的鼓索神经。越来越多的证据表明，钠缺乏也减少了激活的巨噬细胞对舌的切片和对侧完整侧的损伤的反应。由于限钠饮食导致循环醛固酮的强烈增加，我们测试了这样的假设，即CTX对侧的神经生理和免疫反应的变化可以通过醛固酮给药而不是低钠饮食来模拟。CTX和补充醛固酮4-6天的大鼠的味觉反应与CTX和饮食钠限制的大鼠相似。与假手术和补充溶剂的大鼠相比，对钠盐的反应降低了50%。组相关的功能差异被消除与舌应用阿米洛利，表明一个主要的转导途径受影响的是通过上皮钠通道。与功能结果一致，在CTX和醛固酮组大鼠的舌两侧观察到很少的巨噬细胞。相比之下，CTX和溶媒组大鼠舌两侧的巨噬细胞升高。这些结果表明，钠缺乏或醛固酮的管理，抑制神经损伤的免疫反应，导致外周味觉功能减弱。它们还显示了钠失衡、味觉功能和免疫活性的下游后果之间的潜在关键联系。
Guagliardo NA, West KN, McCluskey LP, Hill DL. Attenuation of peripheral salt taste responses and local immune function contralateral to gustatory nerve injury: effects of aldosterone. Am J Physiol Regul Integr Comp Physiol 297: R1103-R1110, 2009. First published August 12, 2009; doi: 10.1152/ajpregu.00219.2009.-Dietary sodium restriction coupled with axotomy of the rat chorda tympani nerve (CTX) results in selectively attenuated taste responses to sodium salts in the contralateral, intact chorda tympani nerve. Converging evidence indicates that sodium deficiency also diminishes the activated macrophage response to injury on both the sectioned and contralateral, intact sides of the tongue. Because a sodium-restricted diet causes a robust increase in circulating aldosterone, we tested the hypothesis that changes in neurophysiological and immune responses contralateral to the CTX could be mimicked by aldosterone administration instead of the low-sodium diet. Taste responses in rats with CTX and supplemental aldosterone for 4-6 days were similar to rats with CTX and dietary sodium restriction. Responses to sodium salts were as much as 50% lower compared with sham-operated and vehicle-supplemented rats. The group-related functional differences were eliminated with lingual application of amiloride, suggesting that a major transduction pathway affected was through epithelial sodium channels. Consistent with the functional results, few macrophages were observed on either side of the tongue in rats with CTX and aldosterone. In contrast, macrophages were elevated on both sides of the tongue in rats with CTX and the vehicle. These results show that sodium deficiency or administration of aldosterone suppresses the immune response to neural injury, resulting in attenuation of peripheral gustatory function. They also show a potential key link among downstream consequences of sodium imbalance, taste function, and immune activity.