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V1-bypassing thalamo-cortical visual circuits in blindsight and developmental dyslexia

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V1-bypassing

thalamo-cortical

visual

circuits

in

blindsight

and

developmental

dyslexia

Samy

Rima

1

and

Michael

Christoph

Schmid

1,2

Visionrestsoncomputationsthatprimarilyrelyonthe

parvocellularandmagnocellulargeniculaterelayofretinal

signalstoV1.Secondarypathwaysinvolvingsuperior

colliculus,koniocellularlateralgeniculatenucleusandpulvinar

andtheirV1-bypassingprojectionstohigherordercortexare

knowntoexist.Whiletheymayformanevolutionaryoldvisual

system,theircontributiontoperceptionandvisuallyguided

behaviourremainlargelyobscure.Recentdevelopmentsin

tracttracingandcircuitmanipulationtechnologiesprovidenew

insights.Herewediscusshowsecondaryvisualpathways

mediateresidualvision(blindsight)afterV1injurybyrelaying

signalsdirectlyintohigherordercorticalareas.Wecontrast

thesefindingsonblindsightwithnewstudiesondyslexia

suggestingthatdysfunctionofsecondaryvisualpathways

mightcontributetodyslexic’sperceptualdifficulties.Emerging

fromtheseconsiderations,secondaryvisualpathways

involvingkoniocellularLGNmaybecriticalfordetectionof

visualchange,whereaspulvinarfunctionappearsmorelinked

tovisuomotorplanning.

Addresses

1Universite´ deFribourg,Switzerland

2

NewcastleUniversity,UnitedKingdom

Correspondingauthors:Rima,Samy(samy.rima@unifr.ch), ChristophSchmid,Michael(michael.schmid@unifr.ch)

CurrentOpinioninPhysiology2020,16:14–20

ThisreviewcomesfromathemedissueonVisionphysiology EditedbyAndrewJParkerandKristineKrug

ForacompleteoverviewseetheIssueandtheEditorial

Availableonline11thMay2020

https://doi.org/10.1016/j.cophys.2020.05.001

2468-8673/ã2020TheAuthors.PublishedbyElsevierLtd.Thisisan openaccessarticleundertheCCBY-NC-NDlicense( http://creative-commons.org/licenses/by-nc-nd/4.0/).

V1-bypassing

thalamo-cortical

visual

circuits

In vision, secondary pathways bypass primary visual cortex (V1) and feed retinal information directly into higher visual cortical areas. The relative strength and contribution of each of these subroutes to perception andvisuallyguidedbehaviourvarywithinthemammals of the Euarchontoglires clade [1] (Figure 1), to which modern primates belong. This variation seems to stem

fromspeciespecific retinal ganglioncell(RGC) organi-zationanddistributionthatemergedfromdifferent eco-logical pressures which, in time, moulded the visual system of each specie. This has led some species of the clade to favour diurnal versus nocturnal lifestyles, with different degrees of front-facing eyes (binocular vision)versusside-facingeyes andmore orless visually guidedgrasping[2].

WhiletheoriginofV1-bypassingroutesundisputedlylies intheretina, theprecisetransferpointsinthemidbrain andthalamusremainanareaofintensestudy,asmultiple subroutesexist.Inmacaques,adedicatedsetofganglion cellsprojectsfromtheretinatoreachthesuperficiallayers ofthesuperiorcolliculus(SC)inthemidbrain[3].From theretwomainparallelprojectionsemergethatbypassV1 [4,5]: one is to the ventral koniocellular/intercalated layersofthelateralgeniculatenucleus(LGN)andfrom theretomultipleareasofvisualassociation,most promi-nentlyarea MT [6–9]; a second projection reaches the inferiorandlateralpartsofthevisualpulvinarand simi-larlyprojectstomultipleareasofvisualassociationcortex

[10–12].InadditiontotheseSCmediatedroutes,certain

ganglioncellsalsoprojectdirectly,withouttheSCdetour, toLGNkoniolayers[8,13,14]and inferiorpulvinar and from there on to visual association areas [15], in both macaquesandmarmosets.Thereisanatomicalevidence thatthestrengthofthepulvinarroutemightbe particu-larlypronetodevelopmentalshapinginmarmosets[16– 19].Animportantsetofelectrophysiologicalrecordingsin LGN and pulvinar has influenced our current under-standingofvisualfunctionintheseregions:LGN record-ings in marmosets established that most dorsal konio neurons aresensitiveto short-wavelengthvisualstimuli [20,21],whereas ventralkonioneurons tendto bemore sensitivetoachromaticstimuliwithlowspatialandhigh temporal frequencies [13,14]. Recordings from the pul-vinarin macaquesestablishedawidesetofvisual func-tions, including responses to faces, snakes [22,23] and saccaderelatedactivitydependingonrecordinglocation

[24–26].AdirectfunctionalconfirmationoftheSC-MT

routevia pulvinar hasbeen established byBerman and Wurtz[11,12]inaseminalstudyusing electrophysiologi-cal collision tests in macaques. In addition to these insightsonahealthy,undisturbedvisualsystem,amajor partofourunderstandingaboutthecontributionsofthese subcorticalstructurestovisualfunctionarisesfrom stud-iesin whichtheprimarygeniculo-V1pathwayhasbeen damaged or inactivated permitting the analysis of V1-bypassing route contributions to residual visual

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function. In this review, we will first describe recent advances from these studies, before contrasting them with new insights on developmental dyslexia in which a V1-bypassing projection has been found to be compromised.

Blindsight

While conscious vision in humans is deeply disrupted followingalesionof V1,significantresidualvisual func-tion remains,[27–31]including thecapacity to execute saccadestowardvisualstimulipresentedwithinthe sco-toma [27,28] and to detect visual motion [29]. This ‘blindsight’ phenomenon hasinstigated alively debate aboutwhichcircuitsthatbypassV1areresponsibleforthe residualvision ofthesepatients. Severalnonhuman pri-mateinvestigationshavedemonstratedsignificant resid-ualneuronalactivityinmotionsensitiveareaMTdespite alesionofV1,consistentwithpreservedmotiondetection capacitiesinblindsight[32–35].Anotherextrastriatearea, V4,whichwasinitiallyshowntobesilencedbyV1cooling [36],appears to regainsome residualactivityin chronic V1 lesions [37]and become moresensitive towardsthe detectionofvisualmotion[38] inmacaques.While itis largely accepted that the SC has a critical function in mediating blindsightbyrelayingvisualsignalsto cortex [32,39], the thalamic relays via LGN versus pulvinar remain atopicofrichdebate [40–42].

For a long time, the LGN route appeared an unlikely candidateduetostrongdegenerationcausedbyV1injury. Butevidenceinmacaquesshowsthatasignificantamount

of cells projecting directly towards visual association cortex survivethis degeneration[9,43].Pharmacological inactivationofLGNneuronseliminatedfunctional acti-vation of visual association cortex and visual detection capacities in a monkey model of blindsight [44]

(Figure2b).Similarinactivationsinpulvinarhadnoeffect

on basic vision but induced neglect-like visuomotor symptoms [45] shifting the focus for blindsight-related circuits further to LGN. Indeed, electrophysiological recordingsfromLGNneuronssurvivingV1lesions con-firmed intact visual processing of these neurons [46]. Modern optogeneticmethodsnowenable theCamK-II specific targeting of koniocellular neurons in an intact visualsystemof macaques,howeverso farwithnoclear delineation of visual response characteristics [47,48]

(Figure 2a). Evidence for the involvement of a

geni-culo-extrastriate pathway in blindsight exists also for humans. In 2015, Ajina et al. [49] used psychophysics andconnectivitymeasurestoshowthatpatientswithV1 lesions that could discriminate motion(blindsight posi-tive) had an intact LGN-hMT+ tract, while those that couldn’tdiscriminatemotion(Blindsightnegative)hada severely impaired or no measurable tracts. The other pathways tested,which includedaconnection between hMT+andthesuperiorcolliculus(SC),andwithhMT+ intheoppositehemisphere,didnotshowthispattern.Ina subsequentstudy,Ajinaetal.[50]usedfMRIto demon-strate that blindsight positive patients had intact func-tionalconnectivitybetweentheLGNandhMT+which was not the case for blindsight negative patients. Fur-thermore,theirresultssuggestthatthiswasspecifictothe

Figure1 LGN Pul SC Extra-striate

Rat Squirrel Tree shrew Galago Marmoset Squirrel

monkey Macaque

SC input Less dense SC input

Dense SC projections Topographic SC projections Retinal projections Retinal terminations Pluv projecting LGN projecting Striate cortex Extrastriate cortex Drosal MT projections (primeres only) Caudal MT 5mm 1mm Dorsal Lateral

Current Opinion in Physiology

OrganizationofsubcorticalstructuresandtheirsubdivisioninvolvedinV1bypassingcircuits.AdaptedfromBaldwinandStates[1].Thevisual systeminhumansfollowscloselytheoverallprimateorganisation[2],butdetailedcircuitinformationisstilllacking.

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LGN,asbothpatientgroupshadpreservedconnectivity between hMT+, the pulvinar and contralateral hMT+. Observationsinhumansthusconfirmedtheexperimental discoveries in V1 lesioned macaques in which residual visualfunction was abolished if theLGN was silenced whichfurtherstrengthenstheinvolvementofa geniculo-extrastriatepathway in blindsight.Althoughkonio neu-ronscanreceiveinputsfromSCaswellasdirectlyfrom theretina[2],itremainstobedeterminedwhichofthese inputsisessentialfor LGN-dependentblindsight. Recentadvancesinchemogeneticandoptogenetic tech-nologieshavehoweveralsobroughtnewgroundbreaking evidencetothePulvinarcontribution.Kinoshitaetal.[51] in an important new study directly tested the role of superior colliculus to ventrolateral pulvinar (vlPul)

pathwayin blindsightmonkeysusingpharmacogenetics

(Figure2c).Theyfirstconfirmedtheabilityofmonkeys

tomakevisuallyguidedsaccadestohighcontraststimuli inthecontralesionalvisualfield.Then,theymappedthe ventralpulvinar byelectricmicrostimulation of theSC. FollowingtheidentificationofthevPul,theyinactivated itthroughtheinjectionofmuscimol.Theprecisionofthe injectionlocation waslater confirmed through Gadolin-ium-based magnetic resonance imaging. This inactiva-tion severely impaired visually guided saccades to the contralesional visualfield.The authors then used phar-maco-genetics to investigate the role of the SC-vPul pathway in the generation of visually guided saccades tothecontralesional visualfield.Theyinjected 2 retro-gradeviral vectors,one in the SC and theother in the vPul. The goal of these injections was to selectively

Figure2 (a) (c) (b) (d) 100 80 60 40 20 0 7 10 17 40 100 % Contrast Correct detection (%) V1 lesioned + LGN inactivated V1 intact V1 lesioned

HiRet injection site

A8 (Monkey-C) M L V D 15 10 5 0 0 –5 –10 –15 15 10 –5 –10 –15 –15 –10 –5 0 –15 –10 –5 0 Horizontal (degree) V e rtical (degree) V e rtical (degree) Horizontal (degree)

Pre (day – 1) Dox (day 12)

Current Opinion in Physiology

InvolvementofK-MTandSC-PUL-MTpathwaysinblindsight.(a)eYFPfluorescenceofKlayersthatexpressCAMKIIandcalbindin.Adaptedfrom Kleinetal.[47].(b)EffectofLGNinactivationonthecorrectdetectionofrotatingcheckerboardswithascotomainducedbyaV1lesion.Adaptedfrom Schmidetal.[44].(c)Injectionsiteoflentiviralvector(HiRet),whichcarriedeTeNTunderthetetracyclineresponsiveelement.(d)Saccadetrajectories andsaccadeendpointsbeforeadministration(Pre)andduringDoxadministration(Dox).(c)and(d)areadaptedfromKinoshitaetal.[51].

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inhibit neurons of the SC-vPul pathway using doxycy-cline.DuringtheoraladministrationofDoxicycline,the accuracy of vision guidedsaccadesto thecontralesional visual field declined and reactiontimes increased.The confirmation of this findingwith similarresultsin mice [52] highlightstheimportanceof thispulvinar routefor re-foveation to high contrast peripheral targets during blindsightacross species.

Thus,thereisgoodevidenceforV1bypassingprojections inblindsightthatimplicateboththeLGNandPulvinar. Intheabsenceofdoubledissociationexperimentsinthe same primatespecies, thereisnoclear-cut answerasto whichofthesesubcorticalpathwaysisultimatelycritical forblindsight.Withpositiveevidenceforeitherroute,the possibility remains that both pathways contribute in parallel with the LGN route possibly more concerned

with basic visual detection and the pulvinar pathway more directlylinkedwithvisuo-motorbehavior.

Developmental

dyslexia

Whilethereisstrongevidencethattheresidualvisualand visuomotorcapacitiesofblindsightrelyonvisualcircuits that bypass V1 into extrastriate cortex, the function of such a circuitry in other clinical contexts – or even everyday vision – remains largely unknown. A recent investigationofsubcorticalcircuitsinsubjectswith devel-opmental dyslexia, however, points to at least one sec-ondary visual pathway bypassing V1 in dyslexia. It is knownthatdyslexicsofdifferentagegroupsandlanguage backgrounds show deficits in visual motion processing [53].Acurrentprominenttheoryascribesthese deficien-cies to a disrupted LGN magnocellular pathway [54].

Figure3

(a)

(c)

(b)

(d) RAN (letters, numbers) Time (s)

Connectivity Index Left V5/MT - LGN

Controls

Dyslexics

Mean functional connectivity (z)

Correlation of timeseries ( r) 0.50 V5 ROI 0.1 0.4 log-normalized nb. streamlines 0.25 0 –0.25 Time 1 Untrained Trained Time 1 Time 1 Time 2 Time 2 –0.50 –0.25 0.00 0.25 0.50 0.75 10 0.15 0.25 0.35 0.45 0.55 0.65 0.75 15 20 25 30 35 Time 2 Controls Dyslexics R2 = .346 p = .045

Trained group

Current Opinion in Physiology

InvolvementofV1bypassingcircuitsinreadingacquisitionandreadingdeficits.(a)DyslexicspresentdecreasedconnectivitybetweenleftLGN andleftareaMT,which(b)negativelycorrelateswithreadingskills.AdaptedfromMu¨ller-axtetal.[56].(c)and(d)Learningtoreadincreases cortico-subcorticalfunctionalconnectivity.AdaptedfromSkeideetal.[66].

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Empirical datafor themagnocellular theoryof dyslexia saw light in 1991 when Livingstone et al. [55] showed that dyslexic subjects had diminished visually evoked potentials to rapid andlow contrast stimuli,but normal responsestoslowandhighcontraststimuli.Investigation ofthepost-mortemdyslexicLGNbyLivingstonrevealed histological abnormalities in the ventral magnocellular layers, but not the dorsal parvocellular layers. Direct evidencefor adeficientvisualpathway bypassingV1 in dyslexics wasrecentlyprovided byMu¨ller-Axt, Anwan-der, and von Kriegstein, [56]. The authors used ultra-high-resolutionfMRIandtractographytoshow reduced structuralconnectivityfromtheleftLGNtoleftmotion area MT with seemingly intact LGN V1 connections

(Figure3a).Thestrength oftheleftLGNMT

connec-tivity was negatively correlated with the rapid naming abilitiesof dyslexics(Figure3b).Thislateralization cor-roboratesrecentanatomicalevidencethatshowsthatthe sizeoftheleftLGNissmallerindyslexicsascomparedto leftLGNofcontrols[57],andalignswithwithreportsof abnormalities in the areas activated during reading in dyslexics [58,59] which are mostly confined in the left hemisphere.fMRIhasshownthatmovingstimulidonot invokethesameactivityinareaMTindyslexicsasitdoes incontrolsubjects[60]withstrongcorrelationsbetween cortical activity, speed discrimination thresholds, and readingspeed[61].Wehaverecentlypartiallyconfirmed thisfinding:thehighersensitivitytodetectvisualmotion intherighthemifieldseeninskilledreaderswasabsentin individuals with developmental dyslexia [62]. Further-more,transcranial directcurrentstimulationof leftarea V5/MT in dyslexics seemsto lead to improvedreading speedandfluency[63],whiletranscranialmagnetic stim-ulation showed that stimulating left area MT lead to impairmentsin wordrecognition[64]. Thereare there-foregoodreasonstolinktheobservedmotiondeficitsin developmental dyslexia to an altered left-hemispheric motionprocessing systeminthebrainofthesesubjects. However,thereisatthemomentsomewhatofa conun-drum about the LGN involvement which will need to be resolved in future research to determine whether the original magnocellular theory should be extended towards koniocellular function, and to what extent the LGN-MT pathway [8] might consist of a mixture of koniocellularand magnocellularinputs.

Comparedtotheevidenceforadeficientlefthemisphere LGN-MTsystemindyslexia,verylittleisknownabout theinvolvement of theother secondary pathway struc-tures.Deheane’sneuronalrecyclinghypothesisproposes thatreadingmakesuseofbrainareasinitiallydevotedto moreprimitivevisualfunctions,andthatthepracticeof readingwouldcarveoutareading networkinthevisual systemthroughplasticity[65].Evidencefor plasticityof subcortical sensory circuits after reading acquisition comes from a recent resting-state fMRI study [66]. Theauthorsshowed(Figure3candd)that,afterlearning

toread for six months,functional connectivity (SC-Pul, subcortical-cortical,lefthemisphere)increasedfor previ-ously illiterate adults. This increased connectivity also correlated with letter identification and word reading skills on the individual level. While the contributions of the SC and the visual pulvinar to developmental Dyslexia remain largely unknown, there is preliminary evidence for pulvinar disruption[67] in addition to the knownLGNdeficit[55].

ThecommonalitiesintheV1-bypassingcircuitsbetween blindsight and developmental dyslexia are intriguing. Furtherinvestigationsusingcell-specificdouble dissoci-ationexperimentsinprimatesshould helptoclarifythe rolesofthepulvinarversusLGNroutes.Drawingupon ourconsiderationsfromblindsightanddyslexia,we spec-ulatethatanticipatoryvisualprocessinginnormalvision, suchasduringreading,mightinvokethedetection prop-erties of the LGN-MT circuit and saccadic planning functionoftheSC-Pulvinarrouteinconcertastovisually locateupcomingobjectssuchaswords,andfurtherguide thefoveafor analysisathighestacuity.

Conflict

of

interest

statement

Nothingdeclared.

Acknowledgement

ThisworkwassupportedbyERCstartinggrant637638OptoVision.

References

1. BaldwinMKL,UnitedStates:TheEvolutionofSubcortical PathwaystotheExtrastriateCortex2017,vol3165-185.

2. KaasJonH:Theevolutionofvisualcortexinprimates.The PrimateVisualSystem.JohnWiley&Sons,Ltd;2006:267-283

http://dx.doi.org/10.1002/0470868112.ch9.

3. PerryVH,CoweyAlan:Retinalganglioncellsthatprojecttothe superiorcolliculusandpretectuminthemacaquemonkey. Neuroscience1984,12:1125-1137http://dx.doi.org/10.1016/ 0306-4522(84)90007-1.

4. HartingJK,HuertaMF,FrankfurterAJ,StromingerNL,RoyceGJ: Ascendingpathwaysfromthemonkeysuperiorcolliculus:an autoradiographicanalysis.JCompNeurol1980,192:853-882.

5. StepniewskaIwona,QiHui-xin,KaasJonH:Dosuperior colliculusprojectionzonesintheinferiorpulvinarprojectto MTinprimates? EurJNeurosci1999,11:469-480http://dx.doi. org/10.1046/j.1460-9568.1999.00461.x.

6. FriesW:Theprojectionfromthelateralgeniculatenucleusto theprestriatecortexofthemacaquemonkey.ProcRSocLond SerB1981,213:73-86.

7. BeneventoL,StandageG:Demonstrationoflackofdorsal lateralgeniculatenucleusinputtoextrastriateareasMTand visual2inthemacaquemonkey.BrainRes1982,252:161-166.

8. SincichLawrenceC,ParkKenF,WohlgemuthMelvilleJ, HortonJonathanC:BypassingV1:adirectgeniculateinputto areaMT.NatNeurosci2004,7:1123-1128http://dx.doi.org/ 10.1038/nn1318.

9. RodmanHR,SorensonKM,ShimAJ,HexterDP:Calbindin immunoreactivityinthegeniculo-extrastriatesystemofthe macaque:implicationsforheterogeneityinthekoniocellular

(6)

pathwayandrecoveryfromcorticaldamage.JCompNeurol 2001,431:168-181.

10. AdamsMichelleM,HofPatrickR,GattassRicardo,

WebsterMareeJ,UngerleiderLeslieG:VisualCorticalProjections andChemoarchitectureofMacaqueMonkeyPulvinar2000,vol 393377-393:(December1999).

11. BermanRebeccaA,WurtzRobertH:Functionalidentificationof apulvinarpathfromsuperiorcolliculustocorticalareaMT. JNeurosci2010,30:6342-6354http://dx.doi.org/10.1523/ JNEUROSCI.6176-09.2010.

12. Anon:Signalsconveyedinthepulvinarpathwayfromsuperior colliculustocorticalareaMT.JNeurosci2011,31:373-384 http://dx.doi.org/10.1523/JNEUROSCI.4738-10.2011.

13. PercivalKA,KoizumiA,MasriRA,BuzasP,MartinPR,GrunertU: Identificationofapathwayfromtheretinatokoniocellular layerK1inthelateralgeniculatenucleusofmarmoset. JNeurosci2014,34:3821-3825http://dx.doi.org/10.1523/ JNEUROSCI.4491-13.2014.

14. EiberCD,RahmanAS,PietersenANJ,ZeaterN,DreherB, SolomonSG,MartinPR:Receptivefieldpropertiesof koniocellularon/offneuronsinthelateralgeniculatenucleus ofmarmosetmonkeys.JNeurosci2018,38http://dx.doi.org/ 10.1523/JNEUROSCI.1679-18.20181679–18.

15. WarnerClaireE,GoldshmitYona,BourneJamesA:Retinal afferentssynapsewithrelaycellstargetingthemiddle temporalareainthepulvinarandlateralgeniculatenuclei. FrontNeuroanat2010,8(4)http://dx.doi.org/10.3389/ neuro.05.008.2010Published2010Feb12.

16. MundinanoInakiCarril,FoxDylanM,KwanWilliamC, VidaurreDiego,TeoLeon,Homman-LudiyeJihane,

GoodaleMelvynA,LeopoldDavidA,BourneJamesA:Transient visualpathwaycriticalfornormaldevelopmentofprimate graspingbehavior.ProcNatlAcadSciUSA2018,115 :1364-1369http://dx.doi.org/10.1073/pnas.1717016115.

17. KwanWilliamC,MundinanoInakiCarril,MitchellJdeSouza, LeeSammyCS,MartinPaulR,Gru¨nertUlrike,BourneJamesA: Unravellingthesubcorticalandretinalcircuitryoftheprimate inferiorpulvinar.JCompNeurol2019,527:558-576http://dx.doi. org/10.1002/cne.24387.

18. Homman-LudiyeJihane,BourneJamesA:Themedialpulvinar: function,originandassociationwithneurodevelopmental disorders.JAnat2019,235:507-520http://dx.doi.org/10.1111/ joa.12932.

19. WarnerClaireE,KwanWilliamC,WrightDavid,JohnstonLeighA, EganGaryF,BourneJamesA:Preservationofvisionbythe pulvinarfollowingearly-lifeprimaryvisualcortexlesions.Curr Biol2015,25:424-434http://dx.doi.org/10.1016/j.

cub.2014.12.028.

20. TailbyC,SzmajdaBA,Buza´sP,LeeBB,MartinPR:Transmission ofblue(S)conesignalsthroughtheprimatelateralgeniculate nucleus.JPhysiol2008,586:5947-5967http://dx.doi.org/ 10.1113/jphysiol.2008.161893.

21. PietersenANJ,CheongSK,SolomonSG,TailbyC,MartinPR: Temporalresponsepropertiesofkoniocellular(Blue-onand Blue-off)cellsinmarmosetlateralgeniculatenucleus. JNeurophysiol2014,112:1421-1438http://dx.doi.org/10.1152/ jn.00077.2014.

22. LeQuanVan,IsbellLynneA,MatsumotoJumpei,NguyenMinh, HoriEtsuro,MaiorRafaelS,TomazCarlos,TranAnhHai, OnoTaketoshi,NishijoHisao:Pulvinarneuronsreveal neurobiologicalevidenceofpastselectionforrapiddetection ofsnakes.ProcNatlAcadSciUSA2013,110:19000-19005 http://dx.doi.org/10.1073/pnas.1312648110.

23. NguyenMinhN,NishimaruHiroshi,MatsumotoJumpei,Van LeQuan,HoriEtsuro,MaiorRafaelS,TomazCarlos, OnoTaketoshi,NishijoHisao:Populationcodingoffacial informationinthemonkeysuperiorcolliculusandpulvinar. FrontNeurosci2016,10http://dx.doi.org/10.3389/

fnins.2016.00583.

24. BenderDB,BaizerJS:Saccadiceyemovementsfollowing kainicacidlesionsofthepulvinarinmonkeys.ExpBrainRes 1990http://dx.doi.org/10.1007/BF00229317.

25. RobinsonDavidLee:Functionalcontributionsoftheprimate pulvinar.ProgBrainRes1993,95:371-380http://dx.doi.org/ 10.1016/S0079-6123(08)60382-9.

26. SchneiderLukas,Dominguez-VargasAdanUlises,GibsonLydia, KaganIgor,WilkeMelanie:Eyepositionsignalsinthedorsal pulvinarduringfixationandgoal-directedsaccades. JNeurophysiol2020,123(1):367-391http://dx.doi.org/10.1152/ jn.00432.2019.

27. Po¨ppelErnst,HeldRichard,FrostDouglas:Residualvisual functionafterbrainwoundsinvolvingthecentralvisual pathwaysinman.Nature1973,243:295-296http://dx.doi.org/ 10.1038/243295a0.

28. WeiskrantzLawrence,WarringtonElizabethK,SandersMD, MarshallJ:Visualcapacityinthehemianopicfieldfollowinga restrictedoccipitalablation.Brain1974,97:709-728http://dx. doi.org/10.1093/brain/97.4.709.

29. BarburJL,RuddockKH,WaterfieldVickiA:Humanvisual responsesintheabsenceofthegeniculo-calcarine projection.Brain1980,103:905-928http://dx.doi.org/10.1093/ brain/103.4.905.

30. StoerigP:Blindsightinmanandmonkey.Brain1997,120 :535-559http://dx.doi.org/10.1093/brain/120.3.535.

31. RadoevaPetyaD,PrasadSashank,BrainardDavidH, AguirreGeoffreyK:NeuralactivitywithinareaV1reflects unconsciousvisualperformanceinacaseofblindsight. JCognitNeurosci2008,20:1927-1939http://dx.doi.org/10.1162/ jocn.2008.20139.

32. RodmanHR,GrossCG,AlbrightTD:Afferentbasisofvisual responsepropertiesinareaMTofthemacaque.I.Effectsof striatecortexremoval.JNeurosci1989,9:2033-2050http://dx. doi.org/10.1017/s0952523800012037.

33. GirardPascal,SalinPA,BullierJ:Responseselectivityof neuronsinareaMTofthemacaquemonkeyduringreversible inactivationofareaV1.JNeurophysiol1992,67:1437-1446 http://dx.doi.org/10.1152/jn.1992.67.6.1437.

34. RosaMG,TweedaleR,ElstonGN:Visualresponsesofneurons inthemiddletemporalareaofnewworldmonkeysafter lesionsofstriatecortex.JNeurosci2000,20:5552-5563http:// www.ncbi.nlm.nih.gov/pubmed/10884339.

35. AzzopardiP,FallahM,GrossC,RodmanH:Responselatencies ofneuronsinvisualareasMTandMSTofmonkeyswithstriate cortexlesions.Neuropsychologia2003,41(13):1738-1756http:// dx.doi.org/10.1016/s0028-3932(03)00176-3.

36. GirardPascal,AntoineSalinPaul,BullierJean:Visualactivityin macaqueareaV4dependsonarea17Input.NeuroReport1991, 2:81-84http://dx.doi.org/10.1097/00001756-199102000-00004.

37. GoebelRainer,MuckliLars,ZanellaFriedhelmE,SingerWolf, StoerigPetra:Sustainedextrastriatecorticalactivationwithout visualawarenessrevealedbyFMRIstudiesofhemianopic patients.VisionRes2001,41:1459-1474http://dx.doi.org/ 10.1016/S0042-6989(01)00069-4.

38. SchmidMichaelC,SchmiedtJoschaT,PetersAndrewJ, SaundersRichardC,MaierAlexander,LeopoldDavidA: Motion-sensitiveresponsesinvisualareaV4intheabsenceofprimary visualcortex.JNeurosci2013,33:18740-18745http://dx.doi.org/ 10.1523/JNEUROSCI.3923-13.2013.

39. MohlerCW,WurtzRH:Roleofstriatecortexandsuperior colliculusinvisualguidanceofsaccadiceyemovementsin monkeys.JNeurophysiol1977,40:74-94.

40. CoweyAlan:Theblindsightsaga.ExpBrainRes2010,200 (1):3-24http://dx.doi.org/10.1007/s00221-009-1914-2.

41. SchmidMichaelC,MaierAlexander:Toseeornottosee -thalamo-corticalnetworksduringblindsightandperceptual suppression.ProgNeurobiol2015,126:36-48http://dx.doi.org/ 10.1016/j.pneurobio.2015.01.001.

(7)

42. BertiniCaterina,GrassoPaoloA,La`davasElisabetta:Theroleof theretino-colliculo-extrastriatepathwayinvisualawareness andvisualfieldrecovery.Neuropsychologia2016,90:72-79 http://dx.doi.org/10.1016/j.neuropsychologia.2016.05.011.

43. CoweyAlan,StoerigP:Projectionpatternsofsurvivingneurons inthedorsallateralgeniculatenucleusfollowingdiscrete lesionsofstriatecortex:implicationsforresidualvision.Exp BrainRes1989,75:631-638http://dx.doi.org/10.1007/

BF00249914.

44. SchmidMichaelC,MrowkaSylwiaW,TurchiJanita,

SaundersRichardC,WilkeMelanie,PetersAndrewJ,YeFrankQ, LeopoldDavidA:Blindsightdependsonthelateralgeniculate nucleus.Nature2010,466:373-377http://dx.doi.org/10.1038/ nature09179.

45. WilkeMelanie,TurchiJanita,SmithKaty,MishkinMortimer, LeopoldDavidA:Pulvinarinactivationdisruptsselectionof movementplans.JNeurosci2010,30:8650-8659http://dx.doi. org/10.1523/JNEUROSCI.0953-10.2010.

46. YuHsin-Hao,AtapourNafiseh,ChaplinTristanA,WorthyKatrina H,RosaMarcelloGP:Robustvisualresponsesandnormal retinotopyinprimatelateralgeniculatenucleusfollowing long-termlesionsofstriatecortex.JNeurosci2018.

47. KleinCarsten,EvrardHenryC,ShapcottKatharineA, HaverkampSilke,LogothetisNikosK,SchmidMichaelC: Cell-targetedoptogeneticsandelectricalmicrostimulationreveal theprimatekoniocellularprojectiontosupra-granularvisual cortex.Neuron2016,90:143-151.

48. HendryS,YoshiokaT:Aneurochemicallydistinctthirdchannel inthemacaquedorsallateralgeniculatenucleus.Science 1994,264:575-577http://dx.doi.org/10.1126/science.8160015.

49. AjinaSara,PestilliFranco,RokemAriel,KennardChristopher, BridgeHolly:Humanblindsightismediatedbyanintact geniculo-extrastriatepathway.eLife2015,4:1-23http://dx.doi. org/10.7554/eLife.08935.

50. AjinaSara,BridgeHolly: In BlindsightReliesonaFunctional ConnectionbetweenHMT+andtheLateralGeniculateNucleus, NotthePulvinar,,vol16.EditedbyPackrsoh.2018http://dx.doi. org/10.1371/journal.pbio.2005769(7).

51. KinoshitaMasaharu,KatoRikako,IsaKaoru,KobayashiKenta, KobayashiKazuto,OnoeHirotaka,IsaTadashi:Dissectingthe circuitforblindsighttorevealthecriticalroleofpulvinarand superiorcolliculus.NatCommun2019,10http://dx.doi.org/ 10.1038/s41467-018-08058-0.

52. BeltramoRiccardo,ScanzianiMassimo:Acollicularvisual cortex:neocorticalspaceforanancientmidbrainvisual structure.Science2019,363:64-69http://dx.doi.org/10.1126/ science.aau7052.

53. PammerKristen:Temporalsamplinginvisionandthe implicationsfordyslexia.FrontHumNeurosci2013,7:933http:// dx.doi.org/10.3389/fnhum.2013.00933.

54. SteinJohn:Themagnocellulartheoryofdevelopmental dyslexia.Dyslexia2001,7:12-36http://dx.doi.org/10.1002/ dys.186.

55. LivingstoneMS,RosenGD,DrislaneFW,GalaburdaAM: Physiologicalandanatomicalevidenceforamagnocellular defectindevelopmentaldyslexia.ProcNatlAcadSciUSA 1991,88:7943-7947http://dx.doi.org/10.1073/pnas.90.6.2556e.

56. Mu¨ller-AxtChrista,AnwanderAlfred,vonKriegsteinKatharina: Alteredstructuralconnectivityoftheleftvisualthalamusin developmentaldyslexia.CurrBiol2017,27:3692-3698.e4http:// dx.doi.org/10.1016/J.CUB.2017.10.034.

57. Giraldo-ChicaMo´nica,HegartyJohnP,SchneiderKeithA: Morphologicaldifferencesinthelateralgeniculatenucleus associatedwithdyslexia.NeuroImageClin2015,7:830-836 http://dx.doi.org/10.1016/j.nicl.2015.03.011.

58. PetersonRobinL,PenningtonBruceF:Developmentaldyslexia. Lancet2012,379:1997-2007 http://dx.doi.org/10.1016/S0140-6736(12)60198-6.

59. RichlanFabio:Developmentaldyslexia:dysfunctionofaleft hemispherereadingnetwork.FrontHumNeurosci2012,6:1-5 http://dx.doi.org/10.3389/fnhum.2012.00120.

60. EdenGF,VanMeterJW,RumseyJM,MaisogJM,WoodsRP, ZeffiroTA:Abnormalprocessingofvisualmotionindyslexia revealedbyfunctionalbrainimaging.Nature1996,382http:// dx.doi.org/10.1038/382066a0.

61. DembJonathanB,BoyntonGeoffreyM,HeegerDavidJ: Functionalmagneticresonanceimagingofearlyvisual pathwaysindyslexia.JNeurosci1998,18:6939-6951http:// www.jneurosci.org/content/jneuro/18/17/6939.full.pdf.

62. RimaSamy,KerbysonGrace,JonesElizabeth,SchmidMichaelC: Advantageofdetectingvisualeventsintherighthemifieldis affectedbyreadingskill.VisionRes2020,169:41-48http://dx. doi.org/10.1016/j.visres.2020.03.001.

63. HethInbahl,LavidorMichal:Improvedreadingmeasuresin adultswithdyslexiafollowingtranscranialdirectcurrent stimulationtreatment.Neuropsychologia2015,70:107-113 http://dx.doi.org/10.1016/j.neuropsychologia.2015.02.022.

64. LaycockRobin,CrewtherDavidP,FitzgeraldPaulB,

CrewtherSheilaG:TMSdisruptionofV5/MT+indicatesarole forthedorsalstreaminwordrecognition.ExpBrainRes2009, 197:69-79http://dx.doi.org/10.1007/s00221-009-1894-2.

65. DehaeneS:ReadingintheBrain:TheNewScienceofHowWe Read.PenguinBook:Science.PenguinBooks;2010https:// books.google.ch/books?id=QyADRQAACAAJ.

66. SkeideMichaelA,KumarUttam,MishraRameshK,TripathiViveka N,GuleriaAnupam,SinghJayP,EisnerFrank,HuettigFalk: Learningtoreadalterscortico-subcorticalcross-talkinthe visualsystemofilliterates.SciAdv2017,3http://dx.doi.org/ 10.1126/sciadv.1602612.

67. GalaburdaAlbertM,EidelbergDavid:Symmetryandasymmetry inthehumanposteriorthalamus:II.Thalamiclesionsinacase ofdevelopmentaldyslexia.ArchNeurol1982,39:333-336http:// dx.doi.org/10.1001/archneur.1982.00510180011002.

Figure

Figure 1 LGN Pul SC  Extra-striate
Figure 2 (a) (c) (b) (d)1008060402007 10 17 40 100% ContrastCorrect detection (%) V1 lesioned+ LGNinactivatedV1 intactV1lesioned

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