Abstract
The primary source of salty taste is Na+ ions, not negatively charged anions paired with them. Experiments on gustatory nerves in animals have shown that anions modulate neural responses to Na+ ions. However, the mechanism of anion modulation remains unclear. The aim of the present study was to determine how anions modulate Na+-induced responses of the bullfrog (Rana catesbeiana) glossopharyngeal nerve (GL). We recorded responses of single fibers of the GL to various Na salts applied to the tongue surface. Since 1 mM NiCl2 enhances the responses of the frog GL to Na salts, 1 mM NiCl2 was always added to 0.01-0.5 M NaCl stimulating solutions. Large anions, such as GMP2−, glutamate− and gluconate−, are unable to pass through the tight junctions between taste cells. Na salts with large anions elicited much smaller responses than did NaCl. They differently and strongly inhibited the responses to NaCl when they were mixed in the NaCl stimulating solutions. The large anions affected the dose-response curve for NaCl in a non-competitive manner. The present findings indicate that the Na+ receptor sites (XNa) responsible for Na+-induced responses reside on the apical membrane of taste cells, not on the basolateral membrane. We hypothesize that anions can differently inhibit the efficacy of Na+-XNa complexes by interacting with anion-binding elements that interact with XNa. [Jpn J Physiol 55 Suppl:S159 (2005)]
