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NH3- and CO2-induced suppression of taste nerve responses in clawed toads and eels

K Yoshii1, C Yotsui

  • 1Dept. of Biochemical Engineering and Science, Kyushu Institute of Technology, Fukuoka, Japan. yoshii@bse.kyutech.ac.jp

Brain Research
|May 23, 1997
PubMed

Insights

Changes in intracellular pH (pHi) by CO2, ammonia, or trimethylamine suppress taste nerve responses in toads and eels. This suppression is linked to altered ion channel or enzyme activity in taste transduction.

Area of Science:

  • Neuroscience
  • Sensory Biology
  • Physiology

Background:

  • Intracellular pH (pHi) plays a crucial role in cellular functions.
  • Taste perception relies on complex signaling pathways involving ion channels and enzymes.

Purpose of the Study:

  • To investigate the impact of altered intracellular pH on taste nerve responses in clawed toads and eels.
  • To determine the specific mechanisms by which chemical stimuli affect taste transduction.

Main Methods:

  • Electrophysiological recordings of taste nerve responses in amphibians and fish.
  • Application of carbon dioxide (CO2), ammonia (NH3), and trimethylamine to alter pHi.
  • Cross-adaptation experiments to identify receptor specificity.

Main Results:

  • CO2, NH3, and trimethylamine reversibly suppressed taste nerve responses to various stimuli in clawed toads.
  • The suppressive effects were non-specific, affecting different receptor sites.
  • Charged species (bicarbonate, carbonate, ammonium) did not suppress responses, indicating the effect is due to the uncharged molecules altering pHi.
  • NH3 altered the threshold and maximum response of L-proline in toads.
  • Similar suppression was observed in eels, with NH3 affecting responses to L-arginine.

Conclusions:

  • Uncharged molecules like CO2, NH3, and trimethylamine suppress taste responses by altering intracellular pH (pHi).
  • CO2-induced acidosis and NH3/trimethylamine-induced alkalosis likely inhibit key ion channels or enzymes involved in taste transduction.
  • These findings elucidate a novel mechanism regulating taste sensitivity through pHi modulation.

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