Olfactory and trigeminal responses to nicotine

Walker, Judy; Kendal-Reed, Martin; Keiger, C. Jane; Bencherif, Merouane; Silver, Wayne L.

doi:10.1002/(sici)1098-2299(199607/08)38:3/4<160::aid-ddr4>3.0.co;2-k

Cited by 33 publications

(21 citation statements)

References 18 publications

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“…In fact, electrophysiological studies in rats (Walker et al, 1996), as well as psychophysical and electrophysiological studies in humans (Thürauf et al, 1999), suggest the existence of a dose-dependent stereoselective activation of the trigeminal sensory system by S(-) and R(+)-nicotine. In the case of reactive substances of varied structures, they could act directly on mucosal tissue, or indirectly by mucosal tissue damage (via chemical reaction) and subsequent release of endogenous chemicals which in turn, would act upon specific ion channels to produce the trigeminal response.…”

Section: Systemmentioning

confidence: 99%

Trigeminal Chemosensation

Cometto‐Muñiz¹,

Doty²

2003

Handbook of Olfaction and Gustation

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Section: Systemmentioning

confidence: 99%

Trigeminal Chemosensation

Cometto‐Muñiz¹,

Doty²

2003

Handbook of Olfaction and Gustation

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“…In the peripheral terminals of trigeminal ganglion (TG) neurons, nicotine activates nAChRs and capsaicin activates TRPV1 receptors (Alimohammadi and Silver 1999;Carstens et al 1998;Jansco et al 1961;Liu and Simon 1996;Sekizawa and Tsubone 1994;Silver and Finger 1991;Steen and Reeh 1993;Tanelian 1991;Walker et al 1996). When they are present in nociceptors, the activation of either of these receptors produces a burning sensation (Dressier et al 1999;DunerEngstrom et al 1986;Green 1989;Jarvik and Assil 1988).…”

Section: Introductionmentioning

confidence: 99%

Nicotine Inhibits Voltage-Dependent Sodium Channels and Sensitizes Vanilloid Receptors

Liu

Zhu

Zhang

et al. 2004

Journal of Neurophysiology

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. Nicotine is an alkaloid that is used by large numbers of people. When taken into the body, it produces a myriad of physiological actions that occur primarily through the activation of neuronal nicotinic acetylcholine receptors (nAChRs). We have explored its ability to modulate TRPV1 receptors and voltage-gated sodium channels. The reason for investigating nicotine's effect on sodium channels is to obtain a better understanding of its anti-nociceptive properties. The reasons for investigating its effects on capsaicin-activated TRPV1 channels are to understand how it may modulate this channel that is involved in pain, inflammation, and gustatory physiology. Whole cell patch-clamp recordings from rat trigeminal ganglion (TG) nociceptors revealed that nicotine exhibited anesthetic properties by decreasing the number of evoked action potentials and by inhibiting tetrodotoxin-resistant sodium currents. This anesthetic property can be produced without the necessity of activating nAChRs. Nicotine also modulates TRPV1 receptors inducing a several-fold increase in capsaicin-activated currents in both TG neurons and in cells with heterologously expressed TRPV1 receptors. This sensitizing effect does not require the activation of nAChRs. Nicotine did not alter the threshold temperature (ϳ41°C) of heat-activated currents in TG neurons that were attributed to arise from the activation of TRPV1 receptors. In this regard, its effect on TRPV1 receptors differs from those of ethanol that has been shown to increase the capsaicin-activated current but decrease the threshold temperature. These studies document several new effects of nicotine on channels involved in nociception and indicate how they may impact physiological processes involving pain and gustation.

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“…Nicotine not only represents the main addictive component of smoking but it also greatly contributes to the sensory properties of tobacco (Laviolette and van der Kooy, 2004;Walker et al, 1996;Hummel et al, 1992a, b;Thuerauf et al, 1999Thuerauf et al, , 2000. The substance presented to the nasal cavity at low concentrations evokes 'odorous' sensations and at higher concentrations 'burning' and 'stinging' sensations, possibly mediated by nicotinic acetylcholine receptors (nAchR) (Walker et al, 1996;Thuerauf et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

“…The substance presented to the nasal cavity at low concentrations evokes 'odorous' sensations and at higher concentrations 'burning' and 'stinging' sensations, possibly mediated by nicotinic acetylcholine receptors (nAchR) (Walker et al, 1996;Thuerauf et al, 1999). In contrast to the majority of other chemical compounds, nicotine activates the olfactory and the trigeminal system at relatively low concentrations (Hummel et al, 1992a, b).…”

Section: Introductionmentioning

confidence: 99%

“…In contrast to the majority of other chemical compounds, nicotine activates the olfactory and the trigeminal system at relatively low concentrations (Hummel et al, 1992a, b). During the last decade stereospecific differences between nicotine enantiomers have been reported for the nasal trigeminal sensory system (Thuerauf et al, 1999(Thuerauf et al, , 2000Walker et al, 1996). S-(À)-nicotineFthe natural isomer of tobaccoFpossesses lower trigeminal thresholds and higher stimulus strength for the 'burning' and the 'stinging' sensation compared to R-( þ )-nicotine.…”

Section: Introductionmentioning

confidence: 99%

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The Influence of Mecamylamine on Trigeminal and Olfactory Chemoreception of Nicotine

Thuerauf

Markovic

Braun

et al. 2005

Neuropsychopharmacol

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Nicotine presented to the nasal cavity at low concentrations evokes 'odorous' sensations, and at higher concentrations 'burning' and 'stinging' sensations. A study in smokers and nonsmokers provided evidence of a relationship between the experience with the pharmacological action of S-(À)-nicotine and the perceived pleasantness/unpleasantness following nasal stimulation with S-(À)-nicotine. Mecamylamine, a nicotinic acetylcholine-receptor-(nAch-R) antagonist, was able to block painful responses following chemical stimulation of the human tongue and to block responses from the rat's ethmoidal nerve. The aim of our study in humans was to investigate the effects of mecamylamine on the olfactory and the trigeminal chemoreception of nicotine enantiomers. In order to achieve this aim, we determinedFbefore and after mecamylamineF(1) detection thresholds, trigeminal thresholds, and intensity estimates (stimulus intensity) and (2) recorded the negative mucosal potential (NMP) following nasal stimulation with nicotine in a placebo-controlled double blind study (n ¼ 15). CO 2 was used as a trigeminal and H 2 S as an olfactory control stimulus. Mecamylamine significantly increased trigeminal thresholds of S-(À)-nicotine and reduced intensity estimates and NMPs following stimulation with nicotine enantiomers, whereas mecamylamine did not influence NMPs and trigeminal intensity estimates following stimulation with CO 2 . In contrast, mecamylamine did neither influence detection thresholds nor olfactory intensity estimates following stimulation with olfactory nicotine concentrations. These results demonstrate that the trigeminal nasal chemoreception of nicotine enantiomers, in contrast to CO 2 , is mediated by nAch-Receptors and give evidence that the olfactory chemoreception of nicotine is independent from peripheral nAchReceptors.

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Olfactory and trigeminal responses to nicotine

Cited by 33 publications

References 18 publications

Trigeminal Chemosensation

Trigeminal Chemosensation

Nicotine Inhibits Voltage-Dependent Sodium Channels and Sensitizes Vanilloid Receptors

The Influence of Mecamylamine on Trigeminal and Olfactory Chemoreception of Nicotine

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