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Taste Exam: A Brief and Validated Test
Published on: August 17, 2018
Signalling mechanisms in mouse bitter responsive taste cells
Masataka Narukawa1, Eiko Minamisawa, Yukako Hayashi
1Graduate School of Agriculture, Kyoto University, Kyoto, Japan.
Insights
Mouse bitter taste perception relies on intracellular calcium (Ca2+) release. This study found that alpha-gustducin and IP3R3 are key components in this bitter transduction pathway.
Area of Science:
- * Neuroscience
- * Cell Biology
- * Sensory Biology
Background:
- * Understanding the molecular mechanisms of taste perception is crucial for sensory biology.
- * Intracellular signaling pathways, particularly involving calcium ions (Ca2+), play a significant role in taste transduction.
Purpose of the Study:
- * To elucidate the components involved in intracellular bitter taste transduction in mice.
- * To investigate the expression patterns of key transduction elements.
- * To determine the contribution of intracellular Ca2+ stores to bitter perception.
Main Methods:
- * Examined the expression of transduction components in taste receptor cells.
- * Utilized immunohistochemistry to identify cells expressing alpha-gustducin and IP3R3.
- * Assessed the impact of intracellular Ca2+ depletion using the inhibitor thapsigargin.
Main Results:
- * 63% of bitter-responsive cells expressed the taste tissue-specific G-protein alpha-gustducin.
- * 78% of alpha-gustducin-positive cells also expressed IP3R3, a receptor for intracellular Ca2+ release.
- * Depleting intracellular Ca2+ stores with thapsigargin abolished bitter responses in 83% of taste cells.
Conclusions:
- * Intracellular Ca2+ release from intracellular stores is a critical step in mouse bitter taste transduction.
- * The G-protein alpha-gustducin and the IP3R3 receptor are integral to this process.
Abstract:
To clarify the components involved in mouse intracellular bitter transduction in the mouse, we investigated the expression patterns of transduction components and the contribution of intracellular Ca2+ stores. Of 64 cells responding to bitter compounds, 63% of the cells expressed the taste tissue-specific G-protein alpha-gustducin. Of the alpha-gustducin immunoreactive cells, 78% expressed IP3R3, a receptor that mediates Ca2+ release from the intracellular store. When intracellular Ca2+ was depleted by treatment with the inhibitor thapsigargin, 83% of the taste cells lost their response to bitter. These data suggest that bitterness transduction involves the release of Ca2+ from intracellular stores.
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