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Chem. Senses 28: 415-422, 2003
© Oxford University Press 2003

Inward currents and increases in cytosolic Ca2+ concentration induced by cyclic ADP-ribose in turtle olfactory receptor cells

Kousuke Sekimoto and Makoto Kashiwayanagi

Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0812, Japan

Correspondence to be sent to: Dr Makoto Kashiwayanagi, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0812, Japan. e-mail: yanagi{at}hucc.hokudai.ac.jp

In olfactory receptor cells, it is well established that cyclic AMP (cAMP) and inositol-1,4,5-trisphosphate (IP3) act as second messengers during odor responses. In previous studies, we have shown that cAMP-increasing odorants induce odor responses even after complete desensitization of the cAMP-mediated pathway. These results suggest that at least one cAMP-independent pathway contributes to the generation of odor responses. In an attempt to identify a novel second messenger, we investigated the possible role of cyclic ADP-ribose (cADPR) in olfactory transduction. Turtle olfactory receptor cells were isolated using an enzyme-free procedure and loaded with fura-2/AM. The cells responded to dialysis with cADPR with an inward current and an increase of the intracellular Ca2+ concentration, [Ca2+]i. Flooding of cells with 100 µM cADPR from the pipette also induced an inward current without changes in [Ca2+]i in Na+-containing and Ca2+-free Ringer solution. In an Na+-free and Ca2+-containing Ringer solution, cADPR induced only a small inward current with a concomitant increase in [Ca2+]i. Inward currents and increases in [Ca2+]i induced by cADPR were completely inhibited by removal of both Na+ and Ca2+ from the outer solution. The experiments suggest that cADPR activates a cation channel at the plasma membrane, allowing inflow of Na+ and Ca2+ ions. The magnitudes of the inward current responses to cAMP-increasing odorants were greatly reduced by prior dialyses of a high concentration of cADPR or 8-bromo-cyclic ADP-ribose (8-Br-cADPR), an antagonist. It is possible that the cADPR-dependent pathway contributes to the generation of olfactory responses.

Key words: Ca2+, cyclic ADP-ribose, inward current, odor response, olfactory cell


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