Mammalian taste buds use ATP as a neurotransmitter. Taste Receptor (type II) cells secrete ATP via gap junction hemichannels into thenarrow extracellular spaces within a taste bud. This ATP excites primary sensory afferent fibers and also stimulates neighboring taste budcells. Hereweshow that extracellularATPis enzymatically degraded to adenosine withinmousevallate taste buds and that this nucleosideacts as an autocrine neuromodulator to selectively enhance sweet taste. In Receptor cells in a lingual slice preparation, Ca 2+mobilizationevoked by focally applied artificial sweeteners was significantly enhanced by adenosine (50 μM). Adenosine had no effect on bitter orumami taste responses, and the nucleoside did not affect Presynaptic (type III) taste cells. We also used biosensor cells to measuretransmitter release from isolated taste buds. Adenosine (50 μM) enhanced ATP release evoked by sweet but not bitter taste stimuli. Usingsingle-cell reverse transcriptase (RT)-PCR on isolated vallate taste cells,weshow thatmanyReceptor cells express the adenosine receptor,Adora2b, while Presynaptic (type III) and Glial-like (type I) cells seldom do. Furthermore, Adora2b receptors are significantly associatedwith expression of the sweet taste receptor subunit, Tas1r2. Adenosine is generated during taste stimulation mainly by the action of theecto-5'-nucleotidase, NT5E, and to a lesser extent, prostatic acid phosphatase. Both these ecto-nucleotidases are expressed by Presynapticcells, as shown by single-cell RT-PCR, enzyme histochemistry, and immunofluorescence. Our findings suggest that ATP releasedduring taste reception is degraded to adenosine to exert positive modulation particularly on sweet taste.
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