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1 Physiology, University of Utah, Salt Lake City, UT, USA
* To whom correspondence should be addressed. E-mail: mary.lucero{at}m.cc.utah.edu.
Although D2 dopamine receptors have been localized to olfactory receptor neurons (ORNs), and dopamine has been shown to modulate voltage-gated ion channels in ORNs, dopaminergic modulation of either odor responses or excitability in mammalian ORNs has not previously been demonstrated. We found that less than 50 µM dopamine reversibly suppresses odor-induced Ca2+ transients in ORNs. Confocal laser imaging of 300 µm thick slices of neonatal mouse olfactory epithelium loaded with the Ca2+-indicator dye fluo-4 AM revealed that dopaminergic suppression of odor responses could be blocked by the D2 dopamine receptor antagonist sulpiride (<500 µM). The dopamine-induced suppression of odor responses was completely reversed by 100 µM nifedipine suggesting that D2 receptor activation leads to an inhibition of L -type Ca2+ channels in ORNs. In addition, dopamine reversibly reduced ORN excitability, as evidenced by reduced amplitude and frequency of Ca2+ transients in response to elevated K+ which activated voltage-gated Ca2+ channels in ORNs. As with the suppression of odor responses, the effects of dopamine on ORN excitability were blocked by the D2 dopamine receptor antagonist sulpiride (<500 µM). The observation of dopaminergic modulation of odor-induced responses in ORNs adds to the growing body of work challenging the longstanding dogma that olfactory receptor neurons are not modulated at the periphery. Dopamine concentrations in nasal mucus increase in response to noxious stimuli, and thus D2 receptor-mediated suppression of voltage-gated Ca2+ channels may be a novel neuroprotective mechanism for ORNs.
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