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Dopamine Reduces Odor- and Elevated-K⁺-Induced Calcium Responses in Mouse Olfactory Receptor Neurons In Situ

Department of Physiology, University of Utah, Salt Lake City, Utah 84108-1297

Submitted 11 July 2003; accepted in final form 1 December 2003

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 <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 activates 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 Ca²⁺ transients in ORNs adds to the growing body of work showing that olfactory receptor neurons can be 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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