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J. Biol. Chem., Vol. 276, Issue 3, 2047-2052, January 19, 2001
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From the Department of Pharmacology, University of Washington,
Seattle, Washington 98195-7280
Olfactory sensory neurons (OSNs) respond acutely
to volatile molecules and exhibit adaptive responses including
desensitization to odorant exposure. Although mechanisms for short term
adaptation have been described, there is little evidence that odorants
cause long lasting, transcription-dependent changes in
OSNs. Here we report that odorants stimulate cAMP-response element
(CRE)-mediated transcription in OSNs through Ca2+
activation of the ERK/MAPK/p90rsk pathway. Odorant stimulation
of ERK phosphorylation was ablated by inhibition of
calmodulin-dependent protein kinase II suggesting that
odorant activation of ERK is mediated through this kinase. Moreover, a
brief exposure in vivo to an odorant in vapor phase stimulated CRE-mediated gene transcription in discrete populations of
OSNs. These data suggest that like central nervous system neurons, OSNs
may undergo long term adaptive changes mediated through CRE-mediated transcription.
Odorants Stimulate the ERK/Mitogen-activated Protein
Kinase Pathway and Activate cAMP-response Element-mediated
Transcription in Olfactory Sensory Neurons*
and
*
This work was supported in part by National Institutes of
Health Grants DC04156 and NS357056.The costs of publication of this article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by National Institutes of Health Training Grant GM07270.
§
To whom correspondence should be addressed: Dept. of Pharmacology,
Mail Box 357280, Health Sciences Bldg., University of Washington, Seattle, WA 98195-7280. Tel.: 206-543-7028; Fax: 206-616-8621; E-mail: dstorm@u.washington.edu.
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