ArticleJournal of neurophysiology2004
Dopamine reduces odor- and elevated-K(+)-induced calcium responses in mouse olfactory receptor neurons in situ.
Article in Journal of neurophysiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 33 citations in OpenAlex.
- Increases in intracellular calcium via activation of potentially multiple phospholipase C isozymes in mouse olfactory neurons.Frontiers in cellular neuroscience · 2014Article
- The β2-adrenergic receptor as a surrogate odorant receptor in mouse olfactory sensory neurons.Molecular and cellular neurosciences · 2014Article
- Presynaptic inhibition of olfactory sensory neurons: new mechanisms and potential functions.Chemical senses · 2013Review
- Peripheral modulation of smell: fact or fiction?Seminars in cell & developmental biology · 2013Review
- Olfactory discrimination varies in mice with different levels of α7-nicotinic acetylcholine receptor expression.Brain research · 2010Article
- The role of the terminal nerve and GnRH in olfactory system neuromodulation.Zoological science · 2009Review
- Defects in neural stem cell proliferation and olfaction in Chd7 deficient mice indicate a mechanism for hyposmia in human CHARGE syndrome.Human molecular genetics · 2009Article
- Olfactory receptor neuron dysfunction in schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2009Article
- Neuroleptic-induced parkinsonism is associated with olfactory dysfunction.Journal of neurology · 2008Article
- Cannabinoid action in the olfactory epithelium.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Terminal nerve-derived neuropeptide y modulates physiological responses in the olfactory epithelium of hungry axolotls (Ambystoma mexicanum).The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
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 microM dopamine reversibly suppresses odor-induced Ca2+ transients in ORNs. Confocal laser imaging of 300-microm-thick slices of neonatal mouse olfactory epithelium loaded with the Ca(2+)-indicator dye fluo-4 AM revealed that dopaminergic suppression of odor responses could be blocked by the D2 dopamine receptor antagonist sulpiride (<500 microM). The dopamine-induced suppression of odor responses was completely reversed by 100 microM 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 microM). 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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