A Quantitative Study of the Enhancing Effect of Nickel Ions on the Taste Response to Sodium Ions of Single Fibers of the Frog Glossopharyngeal Nerve: Competitive Inhibition by Calcium Ions of the Nickel-Enhanced Response to Sodium Ions

Kitada, Yasuyuki; Mitoh, Yoshihiro

doi:10.1093/chemse/21.1.65

Cited by 3 publications

(2 citation statements)

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“…In mixtures of CaCl 2 and NaCl, Na + inhibited the response to Ca 2+ by competing with Ca 2+ for X Ca , whereas Ca 2+ inhibited the response to Na + by competing with Na + for X Na (Kitada 1991). The antagonism remained in the presence of NiCl 2 (Kitada and Mitoh 1996) or after ANS treatment (Kashiwagura et al 1977). These findings suggest that only the binding of each separate cation (agonist) to its appropriate receptor sites leads to the initiation of impulses in water fibers and that enhancers (presence of Ni 2+ and ANS treatment) can enhance the activation of Figure 3 No influence of exposure of the ANS-treated tongue to 10 mM CaCl 2 solution on the enhanced response to 100 mM NaCl.…”

Section: Discussionmentioning

confidence: 95%

“…Because the enhanced responses to NaCl (Kitada 1994d;Kitada and Mitoh 1996) and to choline Cl (Kitada 1994b(Kitada , 1994d induced by the presence of NiCl 2 were observed in water fibers, we examined whether 1 mM ANS treatment can induce enhanced responses of water fibers to NaCl and choline Cl. Figure 7 shows the effects of ANS treatment on water fibers responding to CaCl 2 .…”

Section: Enhancement Of Responses Of Single Water Fibers To Nacl and mentioning

confidence: 99%

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Mechanism of Enhancement of the Responses of the Frog Glossopharyngeal Nerve to Electrolytes by Enhancers

2008

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In frogs, the responses of the glossopharyngeal nerve (GL) to NaCl are enhanced after treatment of the tongue with 8-anilino-1-naphthalene-sulfonic acid (ANS), a hydrophobic probe for biological membranes. The enhancement by ANS treatment has been explained by removal of Ca2+ from the receptor membrane treated with ANS. To explore the mechanism of enhancement by ANS treatment, we recorded neural responses from the frog GL. After ANS treatment, treatment with 10 mM CaCl2 prior to stimulation of NaCl did not affect the enhanced responses to 100 mM NaCl. The response to a relatively high concentration of CaCl2 (50 mM) was enhanced after ANS treatment. It is difficult to interpret these neural events in terms of modulation of the responses by membrane-bound calcium. The presence of NiCl2 in stimulating solution is known as an enhancer. Neural events after ANS treatment were similar to those caused by NiCl2. Our previous studies have demonstrated that enhancement of the responses to electrolytes by NiCl2 is due to modulation of the responses of water fibers in the GL. Water fibers are characterized by sensitivity to water or CaCl2, and they also respond to relatively high concentrations of electrolytes such as NaCl and choline Cl. Using a suction electrode method, we recorded unitary impulses from single water fibers. The ANS treatment led greatly enhanced responses to NaCl or choline Cl in water fibers, suggesting that enhancement by the ANS treatment is due to modulation of the responses of water fibers as well as enhancement by NiCl2. It appears that distinct receptors for each separate cation responsible for the neural responses in water fibers interact with a membrane element that is affected by ANS or Ni2+.

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Section: Discussionmentioning

confidence: 95%

Section: Enhancement Of Responses Of Single Water Fibers To Nacl and mentioning

confidence: 99%

Mechanism of Enhancement of the Responses of the Frog Glossopharyngeal Nerve to Electrolytes by Enhancers

2008

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Enhancing Effect of Nickel Ions on the Response to Magnesium Ions of Single Fibers of the Frog Glossopharyngeal Nerve: Competitive Inhibition by Calcium Ions of the Nickel-enhanced Response to Magnesium Ions

Kitada¹,

Mitoh

1997

Chem Senses

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Single fibers of the frog glossopharyngeal nerve respond to MgCl2 at concentrations exceeding 10 mM. NiCl2 at 1 mM enhanced the Mg2+ response. CaCl2 at 0.5-2 mM induced an inhibition of the Ni(2+)-enhanced response to Mg2+ ions. A quantitative explanation for these results is provided by the hypothesis that Ni2+ ions secondarily affect a magnesium receptor (designated X*Mg) that is responsible for the Mg2+ response and that Ca2+ ions inhibit the Ni(2+)-enhanced response to Mg2+ ions by competing with Mg2+ ions for X*Mg. Double-reciprocal plots of the experimental data indicate that Ni2+ ions do not affect the affinities of X*Mg for both Mg2+ ions (agonist) and Ca2+ ions (competitive antagonist) appreciably, and that Ni2+ ions at 1 mM enhanced the maximal response to Mg2+ ions by 270%. It appears that a magnesium receptor interacts with an Ni(2+)-binding element that is affected by Ni2+ ions and, thus, Ni2+ ions can induce an enhancement of the Mg2+ response.

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Salt Taste Responses in the Frog Glossopharyngeal Nerve: Anion Modulation of Nickel-enhanced Responses to Sodium Ions

2003

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Key words:taste response/sodium salts/anion modulation/nickel ion/fr og glossopharyngeal nerve Abstract:The taste of sodium salts is due to sodium ions . However, the role of anions in salt taste is less well understood. In the present study , we recorded the responses to sodium salts from the frog glossopharyngeal nerve (GL) and explored how anions are involved in salt taste . The frog GL responds to relatively high concentrations of sodium salts (>0 .1M). The order of effectiveness of sodium salts in producing a response was NaCl>Na2SO4>Na gluconate (NaGlu) . It has been reported that addition of 1mM NiCl2 to tastants greatly enhances the responses to NaCl and reduces threshold concentration for NaCl to 0 .02M. In the present study, we used stimulating solutions with 1mM NiCl2 . In the presence of NiCl2, the stimulating effects of NaCl differed markedly from those of Na2SO4 and NaGlu . The order of effectiveness of sodium salts with 1mM NiCl2 was NaCl>>Na2SO4>NaGlu . In the experiments of stimulation with a mixture of NaCl plus other salts in the presence of Ni2+ , we found that gluconate-(Glu-) had an inhibitory effect on the responses to NaCl, whereas SO42-had no effect . Since Glu-(a large anion) is unable to pass through tight junctions between taste cells and only interacts with apical membrane of taste cells , it is likely that Na+-receptor sites (XNa) responsible for the responses to sodium may not reside in the basolateral membra ne, but in the apical receptor membrane. An explanation for these results is provided by the hypothesis that X Na i nteracts with anion-binding element (Y) that is affected by anions and with Ni2+-binding element (T) that is affected by Ni2+. Cl--Y complexes are important for enhancement of the response to Na+ . Gluantagonizes the effect of Cl-. Ni2+ can induce increases in the affinity of Y for Cl-, in the affinity of XNa for Na+ and enhancement of the response to Nat via T.

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A Quantitative Study of the Enhancing Effect of Nickel Ions on the Taste Response to Sodium Ions of Single Fibers of the Frog Glossopharyngeal Nerve: Competitive Inhibition by Calcium Ions of the Nickel-Enhanced Response to Sodium Ions

Cited by 3 publications

References 28 publications

Mechanism of Enhancement of the Responses of the Frog Glossopharyngeal Nerve to Electrolytes by Enhancers

Mechanism of Enhancement of the Responses of the Frog Glossopharyngeal Nerve to Electrolytes by Enhancers

Enhancing Effect of Nickel Ions on the Response to Magnesium Ions of Single Fibers of the Frog Glossopharyngeal Nerve: Competitive Inhibition by Calcium Ions of the Nickel-enhanced Response to Magnesium Ions

Salt Taste Responses in the Frog Glossopharyngeal Nerve: Anion Modulation of Nickel-enhanced Responses to Sodium Ions

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