Bernstein I L, Taylor E M
Department of Psychology, University of Washington, Seattle 98195.
Behav Neurosci. 1992 Aug;106(4):722-5. doi: 10.1037//0735-7044.106.4.722.
Peripheral gustatory mechanisms that may contribute to the expression of sodium (Na) appetite have been a focus of interest for many years. Because amiloride-sensitive Na transport is involved in the generation of neural signals in response to NaCl stimulation, the present study assessed whether changes in amiloride sensitivity of the neural response to NaCl accompany the induction of a Na appetite in the rat. Na deprivation was achieved by acute depletion with the diuretic furosemide. The magnitude of the whole-nerve chorda tympani response to 0.5 M NaCl was reduced in Na-depleted, compared with Na-replete, rats, which provides qualified support for previous reports that the induction of a Na appetite is associated with reduced neural responses to NaCl. However, changes in sensitivity to the specific Na channel blocker amiloride hydrochloride as a result of Na depletion were not evident. These findings suggest that the behavioral and neural changes that occur after Na depletion are not based on changes in amiloride sensitivity in the taste bud.
多年来，可能促成钠（Na）食欲表达的外周味觉机制一直是人们关注的焦点。由于对氯化钠（NaCl）刺激产生的神经信号生成涉及对氨氯地平敏感的钠转运，因此本研究评估了在大鼠诱发钠食欲的过程中，对NaCl的神经反应的氨氯地平敏感性变化是否与之相伴。通过用利尿剂速尿急性耗竭来实现钠缺乏。与钠充足的大鼠相比，钠缺乏的大鼠对0.5M NaCl的鼓索全神经反应幅度降低，这为先前关于诱发钠食欲与对NaCl的神经反应降低相关的报道提供了有力支持。然而，钠缺乏导致的对特定钠通道阻滞剂盐酸氨氯地平敏感性的变化并不明显。这些发现表明，钠缺乏后发生的行为和神经变化并非基于味蕾中氨氯地平敏感性的变化。
