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Olfactory fatigue, also known as odor fatigue, odor habituation, olfactory adaptation, or noseblindness, is the temporary, normal inability to distinguish a particular odor after a prolonged exposure to that airborne compound.^[1] For example, when entering a restaurant initially the odor of food is often perceived as being very strong, but after time the awareness of the odor normally fades to the point where the smell is not perceptible or is much weaker. After leaving the area of high odor, the sensitivity is restored with time. Anosmia is the permanent loss of the sense of smell, and is different from olfactory fatigue.

It is a term commonly used in wine tasting, where one loses the ability to smell and distinguish wine bouquet after sniffing at wine(s) continuously for an extended period of time. The term is also used in the study of indoor air quality, for example, in the perception of odors from people, tobacco, and cleaning agents. Since odor detection may be an indicator that exposure to certain chemicals is occurring, olfactory fatigue can also reduce one's awareness about chemical hazard exposure.

Olfactory fatigue is an example of neural adaptation. The body becomes desensitized to stimuli to prevent the overloading of the nervous system, thus allowing it to respond to new stimuli that are 'out of the ordinary'.^[2]

Mechanism

Odorants are small molecules present in the environment that bind receptors on the surface of cells called olfactory receptor neurons (ORNs).^[3] ORNs are present in the olfactory epithelium which lines the nasal cavity and are able to signal due to an internal balance of signal molecules which vary in concentration depending on the presence or absence an odorant. When odorants bind receptors on ORNs, Ca²⁺ ions flood into the cell causing depolarization and signaling to the brain. Increased Ca²⁺ also activates a negative, stabilizing feedback loop which lowers the olfactory neuron's sensitivity the longer it is stimulated by an odorant to prevent overstimulation. This happens by limiting the amount of cyclic AMP (cAMP) in the cell and by making the Ca²⁺-importing channels which cAMP binds to less responsive to cAMP, both effects reducing further intake of Ca²⁺ and thus limiting depolarization and signaling to the brain. It is important to note that the same mechanism which allows for signaling also limits signaling for prolonged periods of time, the first cannot occur without the second.

On the molecular level, as ORNs depolarize in response to an odorant the G-protein mediated second messenger response activates adenylyl cyclase. This increases cyclic AMP (cAMP) concentration inside the ORN, which then opens a cyclic nucleotide gated cation channel.^[4] The influx of Ca²⁺ ions through this channel triggers olfactory adaptation immediately because Ca²⁺/calmodulin-dependent protein kinase II or CaMK activation directly represses the opening of cation channels, inactivates adenylyl cyclase, and activates the phosphodiesterase that cleaves cAMP.^[5] This series of actions by CaMK desensitizes olfactory receptors to prolonged odorant exposure.^[3]

When the nose is covered taste is a lot harder because the air we breathe goes into the mouth as well. A common idea is that vanilla smells sweet and that is because we taste sweet when we eat vanilla flavorings.^[6]

Mitigating scent effects on olfactory fatigue

According to a study by Grosofsky, Haupert and Versteeg, "fragrance sellers often provide coffee beans to their customers as a nasal palate cleanser" to reduce the effects of olfactory adaptation and habituation. In their study, participants sniffed coffee beans, lemon slices, or plain air. Participants then indicated which of four presented fragrances had not been previously smelled. The results indicated that coffee beans did not yield better performance than lemon slices or air.^[7]

References

^ Binder, M.D.; Hirokawa, N.; Windhorst, U., eds. (2009). "Olfactory Adaptation". Encyclopedia of Neuroscience. Vol. 4. Springer Berlin Heidelberg. p. 2977. doi:10.1007/978-3-540-29678-2_4164. ISBN 978-3-540-23735-8. S2CID 249880749.
^ Kadohisa, Mikiko; Wilson, Donald A. (March 2006). "Olfactory Cortical Adaptation Facilitates Detection of Odors Against Background". Journal of Neurophysiology. 95 (3): 1888–1896. doi:10.1152/jn.00812.2005. PMC 2292127. PMID 16251260.
^ ^a ^b Purves, Dale, ed. (2018). Neuroscience (6th ed.). New York: Oxford University Press. ISBN 978-1-60535-380-7.
^ Chen TY, Yau KW (April 1994). "Direct modulation by Ca(2+)-calmodulin of cyclic nucleotide-activated channel of rat olfactory receptor neurons". Nature. 368 (6471): 545–8. Bibcode:1994Natur.368..545C. doi:10.1038/368545a0. PMID 7511217. S2CID 4342350.
^ Dougherty DP, Wright GA, Yew AC (July 2005). "Computational model of the cAMP-mediated sensory response and calcium-dependent adaptation in vertebrate olfactory receptor neurons". Proceedings of the National Academy of Sciences of the United States of America. 102 (30): 10415–20. Bibcode:2005PNAS..10210415D. doi:10.1073/pnas.0504099102. PMC 1180786. PMID 16027364.
^ Auvray M, Spence C (September 2008). "The multisensory perception of flavor". Consciousness and Cognition. 17 (3): 1016–31. doi:10.1016/j.concog.2007.06.005. PMID 17689100. S2CID 8421312.
^ Grosofsky A, Haupert ML, Versteeg SW (April 2011). "An exploratory investigation of coffee and lemon scents and odor identification". Perceptual and Motor Skills. 112 (2): 536–8. doi:10.2466/24.PMS.112.2.536-538. PMID 21667761. S2CID 34294611.

External links

Kristensen HK, Zilstorff-Pedersen K (December 1953). "Quantitative studies on the function of smell". Acta Oto-Laryngologica. 43 (6): 537–44. doi:10.3109/00016485309119884. PMID 13138121.