2002 Fiscal Year Final Research Report Summary
Signal transduction mechanism of inhibitory responses in vertebrate olfactory receptor neurons
| Project/Area Number |
13640674
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
動物生理・代謝
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| Research Institution | University of Tsukuba |
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Principal Investigator |
NAKATANI Kei University of Tsukuba, Institute of Biological Sciences, Associate Professor, 生物科学系, 助教授 (20125040)
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| Project Period (FY) |
2001 – 2002
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| Keywords | olfactory receptor / inhibitory response / signal transduction / odorant / cAMP / patch-clamp / sensory |
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| Research Abstract |
Although many studies have reported that odorants can elicit inhibitory responses as well as excitatory responses in vertebrate olfactory receptor neurons, the cellular mechanisms that underlie this inhibition are unclear. In this study, we have examined the inhibitory effect of odorants on newt olfactory receptor neurons using whole cell patch-clamp recording.
Odor stimulation caused hyperpolarization and decreased the amplitude of the applied hyperpolarizing voltage, indicating that hyperpolarization was due to a decrease in depolarizing conductance rather than an increase in hyperpolarizing conductance.
Various odorants (anisole, isoamyl acetate, cineole, limonene and isovaleric acid) suppressed the depolarizing current in a dose-dependent manner. The dose-response relation could be fitted by Hill equation : y = E_<max>[X^n / (X^n + IC_<50>^n], where E_<max> is the maximal percentage inhibition and n is the Hill coefficient. The average Hill coefficient was about 1.6.
The mean reversal potential of the conductance suppressed by the odorant was 6.64 ± 1.84 my which was remarkably similar to the conductance induced by IBMX (6.04 ± 2.23 m V,P> 0.68, paired t-test), suggesting that odorant suppressed IBMX-induced current.
Odor stimulation suppressed the IBMX -induced current, suggesting that suppression cannot only be due to competitive effects and that the target of suppression is downstream of receptor binding in the cAMP pathway. The conductance induced by intracellular injection of cAMP was also suppressed by odorants. Odor suppression of the current induced by injection of cAMP demonstrates that the suppression cannot only be caused by inhibition of adenylate cyclase and shows that the target of suppression is after accumulation of intracellular cAMP. Thus, inhibition of the CNG channel seems to be a major cause of suppression of the cAMP-induced current.
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