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Inositol 1,4,5‐trisphosphate and adenophostin analogues induce responses in turtle olfactory sensory neurons
Author(s) -
Kashiwayanagi Makoto,
Tatani Kazuya,
Shuto Satoshi,
Matsuda Akira
Publication year - 2000
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2000.00948.x
Subject(s) - sensory system , inositol , neuroscience , olfactory system , turtle (robot) , biology , chemistry , receptor , biochemistry , ecology
Using the whole‐cell mode of the patch‐clamp technique, we recorded inward currents in response to inositol‐1,4,5‐trisphosphate (IP 3 ) and adenophostin analogues in turtle olfactory sensory neurons. Dialysis of IP 3 into the neurons induced inward currents with an increase in membrane conductance in a dose‐dependent manner under the voltage‐clamp conditions (holding potential −70 mV). The application of Ca 2+ ‐free Ringer solution to neurons previously dialysed with IP 3 induced inward currents that were reversibly inhibited by application of Na + , Ca 2+ ‐free Ringer solution, normal Ringer solution or 10 μ m ruthenium red. Dialysis of the adenophostin analogues, novel IP 3 receptor ligands, also induced inward currents with an increase in membrane conductance. The magnitude of the responses to the adenophostin analogues varied among these derivatives. The application of Ca 2+ ‐free Ringer solution to neurons previously dialysed with the adenophostin analogues induced inward currents that were inhibited by the application of normal Ringer solution. The reversal potential of inward currents induced by an adenophostin analogue was similar to that induced by IP 3 , suggesting that inward currents induced by the adenophostin analogue were generated by a similar ionic mechanism to that induced by IP 3 . The present study demonstrated that IP 3 ‐mediated transduction pathways exist in turtle olfactory receptor neurons and that adenophostin analogues act as agonists of IP 3 .