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alcohol)orphysicalfactors(e.g.,exercise,brightlights)aresomewhatlessprevalentinthepopulation.
Individualswhoreportmultiplenonallergictriggersintheabsenceofallergicreactivityareconsideredto
have “nonallergic rhinitis.” In the absence of another underlying disorder, nonatopic, nasally reactive
individuals have been referred to as having “idiopathic rhinitis,” “vasomotor rhinitis,” “nonallergic,
noninfectious perennial rhinitis”, or “noninfectious, nonallergic rhinitis”. In addition to patients with
nonallergic rhinitis, ~40% of individuals with allergic rhinitis also report reactivity to nonallergic
triggers.
10
Phenotypically, then, so-called nasal hyper-reactivity (defined as nonspecific reactivity to
physical and chemical triggers) is a condition that can affect both atopic and nonatopic individuals.
Beyondsymptomreporting,nasalhyper-reactivityhasbeendefinedfunctionallyinamanneranalogousto
that of bronchial hyper-reactivity (e.g., using challenges with histamine, methacholine, or cold air).
65
Nasal challenge endpoints can include both symptoms (rhinorrhea, nasal blockage) and objective
measures(weightofsecretions,nasalairwayresistance,nasalcross-sectionalarea).Althoughchallenge
testing holds promise, a given individual may exhibit inconsistent reactivity to different test agents,
suggesting a complex underlying pathophysiology. Thus, consensus has yet to emerge regarding the
clinicalutilityofthesestudytechniques.
66
Alsoanalogoustolowerairwaydisease isso-called reactiveupper airwaysdysfunction syndrome
(RUDS).Similartoirritant-inducedasthma,RUDSisaconsequenceofhigh-levelirritantexposure,with
persistent symptoms of airway reactivity (rhinorrhea, nasal obstruction, and nasal hyperesthesia).
67
Although originally defined solely in terms of a one-time, high-level exposure, both irritant-induced
asthmaandrhinitishavealsobeenreportedafterrepeatedexposurestomoremoderatelevelsofirritant.
68
Vocalcorddysfunction(VCD),anotherupperairwayconditionofpotentialreflexorigin,isadisorder
of laryngeal motility in which the vocal folds inappropriately adduct during inspiration rather than
expiration. This results in the sensation of breathlessness, throat pressure, stridor, and hoarseness. A
subsetofpatientswithVCDreporttheonsetofsymptomsafterirritantinhalation,orsymptomstriggered
byodorsandirritants.
69
Pathophysiological mechanisms may includemucosal irritability,motor hyper-
reactivity,orcorticalfactors(e.g.,odorprocessing,conversionreactions).Supportingthepossiblerole
ofmucosalirritabilityisthefactthatbothGERDandpostnasaldripfromrhinosinusitisareriskfactors
for developing VCD.
70
Many individuals with VCD are misdiagnosed as having asthma, leading to
escalatingmedicationdoseswithminimal,ifany,therapeuticresponse.
Odor-triggered panic attacks are another nasal irritant–triggered disorder. In this condition, an
individualisrenderedintoleranttoaspecificchemical'sodorbyvirtueofaone-time,unexpected,high-
levelchemicalexposureatanirritantconcentration(typicallyfarabovetheodorthreshold).Subsequent
to such an incident, the chemical's odor is interpreted as a physical threat. Typical panic symptoms
include breathlessness, perioral and acrodigital paresthesias, lightheadedness, palpitations, a sense of
impendingdoom(anxiety),andasenseofdepersonalizationorderealization.
71
Ifstimulusgeneralization
occurs,thepersonmayreportreactivitytoavarietyofchemicalodors.Therelationshipbetweenasthma
andtwoasthma-likemimics(VCDandpanicattacks)isillustratedinFig. 12.4.In allthreeconditions,
symptoms may be triggered by odorant or irritant exposure, and thus are relevant to a discussion of
trigeminal function.Thethree conditions can exist in isolation or in combination in the same patient.
Diagnostically,itisimportantthatcliniciansconsidernonasthmadiagnoseswhenevaluatingpatientswith
episodic dyspnea triggered by sensorystimuli, especially with symptoms such as inspiratorydyspnea,
upper airway symptoms, or autonomic or central nervous system symptoms. While the diagnostic
approach to asthma is well established, if VCD is suspected, the diagnostic work-up should include
flow–volumeloopsonpulmonaryfunctiontesting,aswellasrhinolaryngoscopytoevaluateforpossible
paradoxical vocal fold motion.
72
Odor-triggered panic attacks are often treated as a diagnosis of
exclusion,afterconsiderationofasthma andVCD.By sharing the differential diagnosisanddiagnostic
logicwiththepatientasthework-upbegins,theclinicianmayavoidthedefensiveresponsethatcanoften
accompanyconsiderationofsomatoformdiagnoses.
Fig.12.4Differentialdiagnosis ofepisodic dyspnea triggeredbyodorantsorirritants.VCD,vocal corddysfunction.(Reproducedwithkind
permissionfromShustermanD.Reviewoftheupperairway,includingolfaction,asmediatorofsymptoms.EnvironHealthPerspect2002;110
(Suppl4):652,withpermission.)
Conclusion
Theintranasaltrigeminalsystemconstitutesathirdchemicalsensenexttosmellandtaste,withwhichitis
intimately connected. There are specific methods to assess sensitivity of the trigeminal system. The
trigeminalsystemmaybeinvolvedinthepathogenesisofseveralsyndromesanddiseases.
Acknowledgments
This publicationwas supported, in part, by a grant toDSfrom FAMRI (the FlightAttendantMedical
Research Foundation); JF is supported by fellowships from FRSQ (Fonds de Recherche en Santé de
Québec)andCIHR(CanadianInstitutesofHealthResearch).
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IISenseofTaste
13FunctionalAnatomyoftheGustatorySystem:FromtheTastePapillatotheGustatoryCortex
14TasteTesting
15TasteDisorders
16BurningMouthSyndromeandQualitativeTasteandSmellDisorders
17StructuralImaginginChemosensoryDysfunction
18ProvidingExpertOpiniononOlfactoryandGustatoryDisorders
19Flavor:InteractionBetweentheChemicalSenses
13FunctionalAnatomyoftheGustatorySystem:FromtheTaste
PapillatotheGustatoryCortex
TatsuKobayakawa,HisashiOgawa
GeneralAspectsofTasteSensation
Tastesensationisoneofthefivesensorymodalities,activatedbychemicalstimulithatreactwithtaste
organsontheoralepithelium.
Fivebasicorfundamentaltastes(i.e.,tastequality)aredescribed;sweet,salty,sour,bitter,andumami.
Sweetnessis caused bysucrose or artificial sweeteners such as saccharin; saltiness solely bysodium
chlorideandlithiumchloride;sournessbyinorganicandorganicacids;bitternessbyvarioussubstances,
suchasureaorquinine;andumamibymonosodiumglutamateandnucleosidemonophosphates.Sweetand
umami represent energy sources or innate rewards; salty, the balance ofminerals; acid, the signal of
putridity;andbitter,thatoftoxins(withsomeexceptions,suchaswhiteleadtastingsweet).
Somespecificareasofthetongueorpalatehavebeenthoughttobemostresponsivetooneparticular
taste,butthishasbeenprovenincorrectandthereislargeindividualvariationintheregionalspecificity
oftasteresponsiveness.
1
Amixtureoftwoormoretastantssometimescausesincreasedordecreasedtastesensationscompared
withthe sumoftasteintensitiescausedbyeachofthecomponenttastantsalone(mixture facilitation or
suppression, respectively).
2
In most cases, this occurs at the peripheral level (e.g., receptor sites).
Mixturefacilitationisseeninsynergisticresponsesbetweentwodifferentumamisubstances.
3
Localizationoftastestimuliispoorcomparedwiththatoftactilestimulation,
1
andisachievedwiththe
aidoftactilesensation.Whenchemicalsareappliedtobothsidesofthetongue,theintensityofthetastant
orthelocationofthesensationchanges,
4
andcentralmechanismsareprobablyinvolvedinthis.
Allaspectsoftastesensationarenotfullystudiedinhumans.Thischapterreviewstastereceptionin
rodents,andneural pathwaysandcoding inmonkeys, onwhichour knowledgeofthe humangustatory
systemislargelybased.Finally,recentfindingsfromnoninvasivestudiesofhumangustatorycorticesare
reviewed.
TasteReception
TasteBuds:TasteReceptorOrgans
Tastebuds(gemmae) aretastereceptororganslocatedonthetongue, palate,andpharynx(Fig. 13.1).
5
Theyare70µminlength,and40µminwidth.Electronmicroscopyrevealsthatatastebudcontains30to
80elongatedcellstogetherwithafewbasalcellsinsidethecapsule.Threedifferenttypesofelongated
cellsareidentified:darkcellsorsupportingcells(typeI;constituting55to75%oftastebudcells),light
cells(typeII;15to30%),andintermediatecells(typeIII;5to15%).Oneortwobasalcells(typeIV)are
alsorecognized(Fig.13.1).
6
TypesI,IIandIIIcellsbearmicrovillithatprojectfromtheapicaldendrites
towardthetastepore(theopeningtotheoralcavity),andareconnectedbytightjunctionsattheapical
dendritessothattastantsandsalivaryfluidcannotaccessthelateralorbasalsurfaceofthecellmembrane
within the taste bud. The taste pore is filled with mucus, but the tip of the microvilli of some cells
projects above this to receive tastants. Type I cells contain secretory granules containing mucous
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substances.TypeIIIcellspossessmicrofilamentssimilartoneurons,makingsynapticcontactswithnerve
terminalsandvarioussynapticvesiclesatthepresynapticarea.
6
TypeIIcellsdonot.
TypeIVcells,situatedatthebaseofthetastebud,areroundwithalobulatednucleus.SometypeIV
cellsexpresstheSonichedgehogprotein, andmaybeatransientprecursoroftypesItoIIIcellsand a
signalcenterfortheproliferationofprogenitorcellsinthetastebuds.
7
Atthe basal pore,a few small
nervefibers(intragemminalfibers)enterthetastebud.
Fig.13.1Tasteorgans.Illustrationshowingtastebuds,thelocationoftastepapillaeonthetongue,andtheirinnervation.1,darkcells;2,light
cells;3,intermediatecells;4,basalcells;CT,chordatympani;GLN,glossopharyngealnerve;SLN,supralaryngealnerve.(FromOgawa.
5
)
Thelifespanofthetastebudcellsisveryshortataround10.5days,
8
althoughamuchlongerlifespanis
notedforsometastereceptorcells.
9
TastePapillae
There are four kindsof papilla on the tongue. Three ofthembear taste buds and are called the taste
papillae(Fig.13.1),althoughtastebudsalsoexistindependentlyinthe epidermisofthesoftpalateor
pharynx.Amongtastepapillae,fungi-formpapillae(0.7to2mmindiameter)arefoundonthe anterior
two-thirdsofthetongueandbearanaverageof3.5tastebudsontop,
10
althoughsomefungiformpapillae
(12.8 to 63%) lack taste budscompletely.
10
Foliate papillae, consisting of as many as 20 ridges and
furrows, are situated on each side of the posterior tongue.
10
Circumvallate papillae, concentrically
groovedstructureswithadiameterof4to8mm,arelocatedinfrontoftheterminalsulcus.Mostpeople
havebetween4and18(averageof9.2±1.8)circumvallatepapillae.
10
Bothfoliateandcircumvallate
papillaebearalargenumberoftastebudsdeepinthetrenchwherethetasteporesopen.Filiformpapillae
bearnotastebudsandarecharacterizedbyacornifiedlayeronthetopoftheepithelium.
Thetotalnumberoftastebudsonthetongueisupto4,600inhumans:24%onfungiformpapillae,28%
onfoliatepapillae,and48% oncircumvallatepapillae.
11
Moretastebudsarelocatedontheposterior
tonguethanontheanteriortongue.
Thedensityoffungiformpapillaeontheanteriortonguecanbeexamined.Itishigh atthetonguetip
(24.5/cm
2
;range2.4to80),butlowonthemediandorsum(8.2/cm
2
;range0to28.3).
11
Thenumberof
tastebudsvariesindividually,and,incontrasttopreviousreports,doesnotdeclinewithage.
11
Patients
whocantastephenylthiocarbamide(PTC)or6-n-propylthiouracil(PROP)havealargernumberoftaste
budsthanthosewhocannot.
11
Thethresholdofdetectionofacertaintastantislowerwhenatonguearea
withahigherdensityoftastebudsisstimulated.
12
Althoughitisreportedthatsinglefungiformpapillaearesensitivetoasinglebasicstimulus,
4
theyare
oftensensitivetoafewtastants.About65%ofpapillaeexaminedhavebeenfoundtobesensitivetoat
leastthreeoffourtastantstested,20%sensitivetoasingletastant,and13%notsensitiveatall.
13
InnervationofTastePapillaeandTasteBuds
Several nerve fibers enter a single fungiform papilla, some of which send collaterals to neighboring
papillae.Thismeansthatasingletastefibercaninnervateseveraltastepapillae.
12
Onaverage,asingle
fiberinnervatesonetofourpapillae.
11
Fungiformpapillaeareinnervatedbythechordatympani(CTN),asensorybranchofthefacialnerve;
foliate papillae by both the CTN and a lingual branch of the glossopharyngeal nerve (GLN); and
circumvallate papillae by the GLN (Fig. 13.1). Taste buds in the soft palate are innervated by the
superficialgreaterpetrosalnerve(SGP),anothersensorybranchofthefacial nerve,while thoseinthe
pharynxareinnervatedbythesupralaryngealnerve,asensorybranchofvagalnerve(VN).
TasteReceptorsandTasteTransduction
TypeIIcellsinthetastebudexpressG-proteincoupledreceptorproteinsforsweet,umami,orbitter,
while type III cells express ionic taste receptors for salty or sour tastants. Taste signals may be
integratedwithinthetastebudsbeforebeingtransmittedtothetastenerves.
Thetastereceptorsforsweet,bitter,andumamiareGprotein–coupledreceptorproteins(GCRPs).They
areseventransmembranedomainreceptorproteinswithanN-terminalintheextracellularspaceandaC-
terminalassociatedwithGproteinintheintracellularspace.Tastereceptorsarebelievedtobelocatedat
theapicalmicrovillioftastereceptorcells(TRCs).Theycanbeclassedastype1(T1R)ortype2(T2R).
T1Rsare class C GCRPswith along N-terminal, whereas T2Rs are class A GCRPswith a shortN-
terminal.
15
T1R1,T1R2,andT1R3arethemselvesorphanreceptorproteins,butaheterodimerofT1R2+
T1R3issweetreceptor,andthatofT1R1+T1R3isumamireceptor(Fig.13.2).
15
Twenty-fiveT2Rsare
involved inreceiving bitter tastants in humans, and different T2Rs are concernedwith different bitter
tastants
15
(e.g.,T2R4for denatonium, T2R38or T2R44 for PTCor PROP, and T2R43 or T2R44for
saccharin).Atasteversionofmetabotropicglutamatereceptortype1or4(tastemGluR1andmGluR4)is
also presumed to be the receptor protein for glutamate, but, unlike T1R1 + T1R3, does not yield
synergisticresponsestoa mixtureofglutamateandribonucleotide.
16
Inthe mouse,T1RsandT2Rsare
expressedindifferentTRCs,butalmostallT2RsareexpressedinthesameTRC.
15
Saltyorsourtastereceptorshavenotbeenfullyelucidated.Thedegenerin/epithelialsodiumchannel
(EnaC) family has been suggested,
16
with the selective amiloride-sensitive ENaC proposed as a
candidate for the salty taste receptor
16
(with no convincing evidence), and a neuronal (degenerin)
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amiloride-sensitive cation channel, including an acid-sensing ion channel (ASCIC), proposed as a
candidatereceptorforsourtaste.
17,18
A heterodimerofpolycystic kidney disease protein1L3and2L1
(PKD2L1)hasalsobeenproposedasthesourreceptor,
15,16
anditsinvolvementinhumansourtastehas
beenreported.
14,15
Fig.13.2Tastereceptor proteins. GPCR,Gprotein–coupledreceptorprotein;T1R,tastereceptortype1;T2R, tastereceptortype2;TRP
channel,transientreceptorpotentialchannel;PKD2L1,polycystickidneydiseaseprotein2L1.(FromChandrashekaretal.
15
)
GCRPsareexpressedintypeIIcells,whereasionicchannelreceptorsforacidorsaltarelocatedin
type III cells.
14,15
Therefore, type II cells are now called receptor cells and type III cells are
presynapticcells.
TasteTransduction
Sodium or lithium ions enter ENaCs to depolarize taste cells, an action that is partly inhibited by
amiloride.Protons(H
+
)activateASCICorPKD2L1toopenanionicchannelanddepolarizecells.
Sweet,bitter,orumamisubstancesreactwithGCRPs,leadingtoactivationofaGprotein(gustducin
inT2Rs
15
), which triggers an intracellular cascade common to TRCs expressing either T1R or T2R:
activation of phospholipase Cβ2; production of inositol-1,4,5-triphosphate; calcium ion release from
intracellularcalciumstores;andfinallystimulationoftransientreceptorpotential(TRP)proteinTRPM5
todepolarizecells(Fig.13.3).
15,16
Transductionofsweettastantisblockedbygymnemicacids.
Type II cells release adenosine triphosphate from pannexin 1 hemichannels, into the intracellular
space, which activates type III cells with purinergic receptors and probably taste nerve fibers by
paracrinesecretion(Fig.13.3).
17
TypeIIIcellsactivatetastefiberterminalsviasynapses.Thus,typeIII
cells as well as taste fibers are able to respondtoorganic tastants.
17
Chemicals such as serotonin or
glutamatehavebeensuggestedassynaptictransmittersbetweentypeIIIcellsandnerveterminals.
18,19
Temperature dependence of taste transduction has been noted in taste psychophysics
20
and the
physiology oftastefibers.
21
Mosttasteresponseshaveanoptimal temperature of30°C,exceptsodium
chloride,whichhasanoptimaltemperatureof10°Corlower,suggestingthepresenceofanenergybarrier
forchemicalreactionsbetweentastantsandreceptors.However,itispartiallyascribedtothetemperature
dependenceofTRPM5.
22
ResponsivenessofTasteReceptorCells
Electrophysiology has shown that TRCs generate depolarizing receptor potentials in response to
tastants,
23
butcanalsoproducesodiumspikesbecauseofthepresenceofsodiumchannels.
24
Inmice,type
II cells differentially respond to umami, sweet, or bitter, while type III cells respondto salt or sour
tastants.
16
Fig. 13.3 Intracellular and intercellular signaling in taste bud cells. II, type II cell; III, type III cell; 5-HT, serotonin; ATP, adenosine
triphosphate; GCRP, G protein–coupled receptor protein; Glu, glutamate; IP3, inositol-3 phosphate; PLCβ2, phospholipase Cβ2; TRPM5,
transientreceptorpotentialproteinM5;Ca,calciumions.
PeripheralTasteNerves
CourseofTasteNerves
TheCTNandSGPtakeaperipheralcoursetowardthetastebuds,togetherwiththelingualbranch(LN)
orpalatalbranchofthetrigeminalnerve.Theytakeacomplexcentralcoursetothemedullatoterminate
inthesolitarytractnucleus(NTS)(Fig.13.4).
The CTNtravels tothe tympanic cavity,where itruns nearthe auditory ossicles. It thenenters the
facialcanaltoformthegeniculateganglion,andtofusewiththeSGPtoformtheintermediatenerveof
Wrisberg (IMN), which joins the facial nerve. After leaving the soft palate, the SGP traverses the
sphenopalatine gangliontothetympanic cavity,with itscell body inthegeniculateganglion.TheIMN
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