contributes to nAChR agonist binding and de-sensitization kinetics (8), but also may respondto changes in network activity (34). Local reg-ulation of Lynx1 levels may allow cholinergicactivation to induce islands of plasticity whilemaintaining overall circuit stability. Visual at-tention tasks in fact preferentially modulate fast-spiking inhibitory neurons (35, 36), consistentwith a convergence of top-down influences uponlocal excitatory-inhibitory circuit balance.

References and Notes1. T. K. Hensch, Annu. Rev. Neurosci. 27, 549 (2004).2. B. A. Wandell, S. M. Smirnakis, Nat. Rev. Neurosci. 10,

873 (2009).3. H. Morishita, T. K. Hensch, Curr. Opin. Neurobiol. 18,

101 (2008).4. T. Pizzorusso et al., Science 298, 1248 (2002).5. A. W. McGee, Y. Yang, Q. S. Fischer, N. W. Daw,

S. M. Strittmatter, Science 309, 2222 (2005).6. J. Syken, T. Grandpre, P. O. Kanold, C. J. Shatz, Science

313, 1795 (2006).7. C. Plessy et al., PLoS ONE 3, e3012 (2008).8. J. M. Miwa et al., Neuron 23, 105 (1999).9. I. Ibañez-Tallon et al., Neuron 33, 893 (2002).

10. J. A. Davis, T. J. Gould, Psychopharmacology (Berl.) 184,345 (2006).

11. J. M. Miwa et al., Neuron 51, 587 (2006).12. A. A. Disney, C. Aoki, M. J. Hawken, Neuron 56, 701 (2007).13. G. T. Prusky, C. Shaw, M. S. Cynader, Brain Res. 412,

131 (1987).14. D. Parkinson, K. E. Kratz, N. W. Daw, Exp. Brain Res. 73,

553 (1988).15. Z. Gil, B. W. Connors, Y. Amitai, Neuron 19, 679 (1997).16. I. Kruglikov, B. Rudy, Neuron 58, 911 (2008).17. E. Lucas-Meunier et al., Cereb. Cortex 19, 2411 (2009).18. M. C. Kuo, D. D. Rasmusson, H. C. Dringenberg,

Neuroscience 163, 430 (2009).19. P. Aracri et al., Cereb. Cortex 20, 1539 (2010).20. M. Alkondon, E. F. R. Pereira, H. M. Eisenberg,

E. X. Albuquerque, J. Neurosci. 20, 66 (2000).21. E. O. Mann, I. Mody, Curr. Opin. Neurol. 21, 155 (2008).22. R. Satta et al., Proc. Natl. Acad. Sci. U.S.A. 105,

16356 (2008).23. Q. Gu, W. Singer, Eur. J. Neurosci. 5, 475 (1993).24. J. L. Herrero et al., Nature 454, 1110 (2008).25. M. Goard, Y. Dan, Nat. Neurosci. 12, 1444 (2009).26. J. I. Kang, E. Vaucher, PLoS ONE 4, e5995 (2009).27. D. M. Levi, R. W. Li, Philos. Trans. R. Soc. Lond. B Biol.

Sci. 364, 399 (2009).28. M. W. Dye, C. S. Green, D. Bavelier, Neuropsychologia

47, 1780 (2009).29. M. A. Silver, A. Shenhav, M. D’Esposito, Neuron 60,

904 (2008).30. R. F. Hess, B. Thompson, G. Gole, K. T. Mullen, Eur. J.

Neurosci. 29, 1064 (2009).

31. P. Lempert, Ophthalmic Physiol. Opt. 25, 592(2005).

32. M. Sarter, M. E. Hasselmo, J. P. Bruno, B. Givens, BrainRes. Brain Res. Rev. 48, 98 (2005).

33. M. F. Bear, W. Singer, Nature 320, 172 (1986).34. C. K. Pfeffer et al., J. Neurosci. 29, 3419 (2009).35. J. F. Mitchell, K. A. Sundberg, J. H. Reynolds, Neuron 55,

131 (2007).36. Y. Chen et al., Nat. Neurosci. 11, 974 (2008).37. We thank M. Fagiolini, H.A. Lester, and A. Takesian for their

helpful comments on the manuscript and M. Marcotrigianofor animal maintenance. This study was supported by theJames S. McDonnell Foundation “Recovery from Amblyopia”network (T.K.H.), NIH Director’s Pioneer Award (1 DP1 OD003699-01 to T.K.H.), the Ellison Medical Foundation (T.K.H.),Howard Hughes Medical Institute (N.H.), DA-17279 andCalifornia Tobacco-Related Disease Research Program ( J.M.M.),and the Japanese Society for Promotion of Science (H.M.)

Supporting Online Materialwww.sciencemag.org/cgi/content/full/science.1195320/DC1Materials and MethodsFigs. S1 to S3References

19 July 2010; accepted 28 September 2010Published online 11 November 2010;10.1126/science.1195320

Motor Control by Sensory CortexFerenc Matyas,1,2 Varun Sreenivasan,1 Fred Marbach,1 Catherine Wacongne,1,3 Boglarka Barsy,1,4

Celine Mateo,1 Rachel Aronoff,1 Carl C. H. Petersen1*

Classical studies of mammalian movement control define a prominent role for the primary motor cortex.Investigating the mouse whisker system, we found an additional and equally direct pathway for corticalmotor control driven by the primary somatosensory cortex. Whereas activity in primary motor cortexdirectly evokes exploratory whisker protraction, primary somatosensory cortex directly drives whiskerretraction, providing a rapid negative feedback signal for sensorimotor integration. Motor control bysensory cortex suggests the need to reevaluate the functional organization of cortical maps.

The remarkable findings of Penfield andBoldrey (1), which have been supportedby many subsequent studies (2–11), em-

phasize a key role formotor cortex inmammalianmovement control. Investigating themouse whiskersystem (12–14), we found that primary somato-

sensory barrel cortex forms an equally direct andequally prominentmotor control pathway, comparedwith that originating from the classical motor cortex.

We first functionally mapped the sensory ac-tivity evoked by a single brief deflection of the C2whisker through wide-field voltage-sensitive dye

(VSD) imaging of the contralateral sensorimotorcortex in awake head-restrained mice (15, 16).The earliest cortical VSD response to C2 whiskerdeflection occurred at 7.4 T 0.5 ms (n = 5 mice,mean T SD) and was specifically localized to theC2 barrel column of primary somatosensory neo-cortex (S1C2) (Fig. 1A). Over the subsequent mil-liseconds, nearby cortical columns depolarized,with activity propagating in a wavelike manner.

Fig. 4. Lynx1 may adjustcortical excitatory-inhibitorybalance to regulate adultplasticity. (A) InWT animals(left), mature excitatory-inhibitory balance ismain-tained by Lynx1 that limitsnAChR response. In Lynx1KO mice (right), enhancednAChR signaling may leadto excitatory-inhibitory im-balance and adult plastici-ty, which could be sensitiveto acute restoration of inhi-bition with diazepam (DZ).(B) Double in situ hybrid-ization of Lynx1 (green)withGAD65 (red, top) or parv-albumin (PV, bottom) in adult V1 (left). Scale bar, 100 mm. Quantification of over-lapping pixels (right) indicates selective expression of Lynx1 in a subset (40%) ofGAD65-positive interneurons, most likely PV-positive cells (>90% colocalization). (C)

Focal diazepam infusion during adult MD in Lynx1 KO mice abolishes oculardominance plasticity (black, DZ: CBI = 0.67, 6 mice versus gray, vehicle (Veh): CBI =0.54, 14mice; ***P<0.001, t test). Dark circles represent corticalminipump infusion.

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1Laboratory of Sensory Processing, Brain Mind Institute, Facultyof Life Sciences, École Polytechnique Fédérale de Lausanne(EPFL), CH-1015 Lausanne, Switzerland. 2Laboratory of Thal-amus Research, Institute of Experimental Medicine, HungarianAcademy of Sciences, H-1450 Budapest, Hungary. 3CognitiveNeuroimaging Unit, INSERM U992, F-91191 Gif-sur-Yvette,France. 4Institute of Experimental Medicine, Hungarian Academyof Sciences, H-1450 Budapest, Hungary.

*To whom correspondence should be addressed. E-mail:carl.petersen@epfl.ch

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At 6.5 T 1.9 ms (n = 5 mice) after the firstexcitation of the C2 barrel column, a second lo-calized region of depolarization was evoked inprimary motor cortex (M1C2), which also spreadover the next milliseconds (Fig. 1A). These im-aging experiments defined two spatially local-ized initiation sites (S1C2 and M1C2) for corticalsensory processing associatedwith theC2whisker.To gain insight into their functional contribu-tions to whisker behavior, we targeted intracor-tical microstimulation (ICMS) to these two corticalregions, finding that stimulation of either S1C2 orM1C2 evoked short-latency retraction of the C2whisker (n = 5 mice) (Fig. 1B). Stimulation of amore medial region of motor cortex (M1Protract)drove rhythmic whisker protraction (Fig. 1B). Ad-ditional mapping experiments based on stereotaxiccoordinates revealed this motor map to be welldefined, with M1C2 localized within the motorcortex whisker retraction area, M1Retract (figs. S1and S2) (8, 15). Quantified across all experiments(Fig. 1C), ICMS of S1C2 drove whisker retractionof –10.3° T 3.9° with a latency of 14.8 T 2.8 ms(n = 26, stimulation sites across 26 mice); ICMSof M1Retract drove whisker retraction of –18.0° T8.8°with a latency of 21.1 T 5.8ms (n=116, across31 mice); and ICMS of M1Protract drove whiskerprotraction of 17.1° T 9.0° with a latency of 35.3 T12.1 ms (n = 86, across 30 mice). Latencies forevokingwhiskermovementswere shorter for ICMSof S1 compared with those of M1 (P < 0.001).

Fig. 1. Cortical sensorimotorinteractions in the mousewhisker system. (A) VSD im-aging reveals the spatio-temporal dynamics of thecortical sensory responseevoked by a single brief de-flection of the C2 whisker.(B) ICMS (gray shading) ofS1C2 (red) and M1C2 (blue)evoked whisker retraction,whereas ICMS of M1Protract(green) drove whisker pro-traction. (C) Movement am-plitude and latency evokedby ICMS of S1C2 (n=26mice),M1Retract (including M1C2, n =31 mice), and M1Protract (n =30 mice). (D and E) Sensory-evoked whisker retraction(yellow) was blocked by TTXinactivation of S1 (orange)(P < 0.01, n = 5mice). Datapresented as mean T SD.

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Thus, the cortical regions involved in the initialprocessing of C2 whisker sensory input (S1C2 andM1C2) both drove whisker retraction. To test for be-havioral relevance of the retraction motor responsefrom sensory cortex, we attached metal particles tothe C2 whisker and evoked a train of brief whiskerdeflections by a pulsed magnetic field. Mice re-tracted the C2 whisker in response to this sensorystimulus by –2.8° T 1.4° (n = 5 mice), but, if the S1barrel cortexwas inactivated by tetrodotoxin (TTX),then the mice failed to respond (whisker movementof 0.3°T 1.2°,n=5mice,P<0.01) (Fig. 1,DandE).Inactivation of motor cortex by TTX did not af-fect the sensory-evokedwhisker retraction (fig. S3).

These results suggest that S1might drivemove-mentwithout the participation ofM1.We tested thishypothesis by investigating the effect of TTX ap-plication to M1 on ICMS-evoked movements. Al-though complete blockade of motor cortex wasverified by the absence of movements evoked byICMS of M1, the whisker retraction evoked byICMS of S1 was unaffected by TTX application toM1 (control amplitude of –11.0° T 3.4°, TTXM1

amplitude of –11.6° T 2.1°; control latency 13.0 T1.5 ms, TTXM1 latency 12.9 T 1.6 ms; n = 7 mice)(Fig. 2, A and B).

ICMS evokes widespread activity under someexperimental conditions (15, 17, 18). We there-fore tested for S1-evoked movements by using asecond independent method that involved opto-genetic stimulation of neurons expressing ChR2(19, 20). In Thy1-ChR2 transgenic mice (21, 22),robust whisker retraction could be evoked by bluelight stimulation of S1 barrel cortex (Fig. 2C).Application of TTX to motor cortex completelyblocked movements evoked by optogenetic stim-ulation of motor cortex, but it had no effect uponS1-evoked optogenetic whisker retraction (S1 con-trol amplitude –15.5° T 2.7°, S1 TTXM1 ampli-tude –12.7° T 0.9°; S1 control latency 13.7 T 0.9ms, S1 TTXM1 latency 14.3 T 0.9 ms; n = 5 mice)(Fig. 2, C and D, and movie S1). To achieve thehighest specificity for optogenetic stimulation, weused an adeno-associated viral (AAV) vector tolocally express ChR2 in S1 barrel cortex (Fig. 2E).Blue light stimulation of these S1 neurons drove arobust short-latency whisker retraction in 8 out of11 mice (amplitude –10.8° T 3.2°, latency 16.1 T1.8 ms, n = 8 mice) (Fig. 2, E and F).

We next began to question whether the move-ments evoked by stimulation of M1 were drivendirectly by motor cortex or whether the evokedwhisker retractionmight actually be relayed via S1.Whisker protraction driven by ICMS of M1Protractwas enhanced by TTX inactivation of S1 (n = 13mice) (Fig. 3, A and B). However, the whisker re-traction evoked under control conditions by ICMSofM1Retractwas reversed after TTXapplication toS1and was replaced by rhythmic protraction (controlamplitude –18.0° T 5.6°, TTXS1 amplitude 21.6° T9.9°, n = 14 mice) (Fig. 3, A and B). Similarly,the retraction evoked by optogenetic stimulation ofM1Retract in Thy1-ChR2micewas also reversed intoprotraction by TTX application to S1 (n = 5 mice)(Fig. 3, C andD, andmovie S2). In a separate set of

experiments, applying 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) andD-2-amino-5-phosphonovalericacid (APV) to S1 [to block AMPA and N-methyl-D-aspartate (NMDA) types of ionotropic glutamatereceptors, respectively], we determined that thewhisker retraction evokedbyoptogenetic stimulationof M1Retract is mediated by a glutamatergic synapsein S1, whereas neither the protraction evoked bystimulation ofM1Protract nor the retraction evoked bystimulation of S1 required glutamatergic synaptictransmission in S1 (Fig. 3, E and F). These resultsreveal that the direct action of whisker primary

motor cortex neurons (bothM1Retract andM1Protract)is to drive whisker protraction. The whisker retrac-tion evoked by stimulation of motor cortex areaM1Retract is in fact driven indirectly, but reliably, viasynaptic activation of S1.

Having defined different functional motor rolesfor M1 (whisker protraction) and S1 (whisker re-traction), we next investigated the downstreamsignaling pathways. Consistent with amajor feed-forward pathway for sensory information from S1to M1 visualized with VSD (Fig. 1), we found ahigh-density column of axons from S1C2 in the

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Fig. 3. Whisker retraction evoked by stimulation of motor cortex is driven by sensory cortex. (A and B)Inactivation of S1 enhanced whisker protraction evoked by ICMS of M1Protract (green, n=13mice, P<0.01), butin the same mice it reversed the movements evoked by ICMS of M1Retract (blue, n = 14 mice, P < 0.001) fromretraction into protraction. (C and D) Whisker retraction evoked by optogenetic stimulation of M1Retract in Thy1-ChR2 transgenic mice was also changed into whisker protraction after S1 inactivation by TTX (P < 0.01, n = 5mice). (E and F) Application of CNQX and APV to S1 did not affect whisker movements evoked by optogeneticstimulation of S1 (red; n= 4mice) or M1Protract (green; n= 3mice), but whisker retraction driven by optogeneticstimulation ofM1Retract was changed into protraction (blue; P<0.01, n=4mice). Data presented asmean T SD.

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location ofM1C2 (Fig. 4A) (15, 23). The reciprocalaxonal projection fromM1C2 preferentially innerva-ted L1 and L5/6 of the S1 barrel field (S1-BF) andthe neighboring dysgranular zone (S1-DZ) (Fig. 4B)(24). Whereas the corticocortical projections ofS1C2 andM1C2were quite different fromeachother,the overallmap of subcortical projections followeda similar pattern. Both S1C2 and M1C2 strongly in-nervated adjacent (but mainly nonoverlapping)brain regions involved in processing whisker sen-sation and movement, that is, dorsal striatum, thal-amus, superior colliculus, red nucleus, pontine nuclei,and trigeminal brainstem (Fig. 4C and fig. S4).

Whisker movements evoked by motor cortexstimulation are likely mediated by the prominentM1C2 innervation of the brainstem reticular for-mation (RF) (Fig. 4C), which projects heavily intothe facial nucleus (FN), where the whisker motorneurons are located (25, 26). In an analogous paral-lel pathway, the most prominent brainstem pro-jection of S1C2 is to the spinal trigeminal nuclei(SP5) (Fig. 4C) (23, 27), which project strongly tothe facial nucleus (25, 28). Direct electrical stim-ulation of SP5 evoked whisker retraction (ampli-tude –5.1° T 8.5° , latency 6.5 T 1.8 ms, n = 4mice), whereas stimulation of RF drove whiskerprotraction (amplitude 14.4° T 12.9°, latency 5.4 T1.7 ms, n = 3 mice) (Fig. 4, D and E). We thuspropose the existence of two parallel motor sig-naling pathways, which emerge from distinct cor-tical areas (M1 and S1) and are relayed via distinctnuclei in the brainstem (RF and SP5) to antagonis-tic pools of motor neurons in FN driving differentwhisker-related muscles (29): M1 drives whiskerprotraction (M1 → RF → FN), and S1 driveswhisker retraction (S1→ SP5→ FN) (Fig. 4F).

We found evidence for a strong and direct roleformouse sensory cortex inwhiskermotor control.

Given the importance of sensorimotor interactionsduring any form of active sensing, one should nextexamine whether reliable and direct motor controlby sensory cortex is a general feature or whether itis a specialization of the mouse whisker sensori-motor system. Interestingly, previous investigationsfound overlapping sensory and motor representa-tions of the rodent hindlimb (2). Furthermore, inthe monkey, corticospinal neurons are present inS1 (30), and retrograde trans-synaptic tracing fromfinger muscles labels neurons in S1 (31). In thiscontext, it is also interesting to note that earlymotor mapping studies in monkeys (32) and hu-mans (1) describe movements evoked by stimula-tion of primary somatosensory cortex in additionto motor cortex. Motor control by sensory cortex,as demonstrated by our experiments in the mousewhisker system,might therefore also be relevant tothe functional organization of human cortex.

References and Notes1. W. Penfield, E. Boldrey, Brain 60, 389 (1937).2. J. P. Donoghue, S. P. Wise, J. Comp. Neurol. 212, 76 (1982).3. A. P. Georgopoulos, A. B. Schwartz, R. E. Kettner, Science

233, 1416 (1986).4. J. Wessberg et al., Nature 408, 361 (2000).5. M. D. Serruya, N. G. Hatsopoulos, L. Paninski,

M. R. Fellows, J. P. Donoghue, Nature 416, 141 (2002).6. M. S. Graziano, C. S. Taylor, T. Moore, Neuron 34, 841 (2002).7. M. Brecht, M. Schneider, B. Sakmann, T. W. Margrie,

Nature 427, 704 (2004).8. F. Haiss, C. Schwarz, J. Neurosci. 25, 1579 (2005).9. D. A. Dombeck, M. S. Graziano, D. W. Tank, J. Neurosci.

29, 13751 (2009).10. Y. Isomura, R. Harukuni, T. Takekawa, H. Aizawa, T. Fukai,

Nat. Neurosci. 12, 1586 (2009).11. T. Komiyama et al., Nature 464, 1182 (2010).12. M. Brecht, Curr. Opin. Neurobiol. 17, 408 (2007).13. C. C. H. Petersen, Neuron 56, 339 (2007).14. M. E. Diamond, M. von Heimendahl, P. M. Knutsen,

D. Kleinfeld, E. Ahissar, Nat. Rev. Neurosci. 9, 601 (2008).15. I. Ferezou et al., Neuron 56, 907 (2007).

16. Materials and methods are available as supportingmaterial on Science Online.

17. E. Seidemann, A. Arieli, A. Grinvald, H. Slovin, Science295, 862 (2002).

18. M. H. Histed, V. Bonin, R. C. Reid, Neuron 63, 508 (2009).19. G. Nagel et al., Proc. Natl. Acad. Sci. U.S.A. 100,

13940 (2003).20. E. S. Boyden, F. Zhang, E. Bamberg, G. Nagel,

K. Deisseroth, Nat. Neurosci. 8, 1263 (2005).21. B. R. Arenkiel et al., Neuron 54, 205 (2007).22. O. G. Ayling, T. C. Harrison, J. D. Boyd, A. Goroshkov,

T. H. Murphy, Nat. Methods 6, 219 (2009).23. R. Aronoff et al., Eur. J. Neurosci. 31, 2221 (2010).24. P. Veinante, M. Deschênes, J. Comp. Neurol. 464, 98 (2003).25. A. M. Hattox, C. A. Priest, A. Keller, J. Comp. Neurol. 442,

266 (2002).26. L. J. Herfst, M. Brecht, J. Neurophysiol. 99, 2821 (2008).27. M. F. Jacquin, M. R. Wiegand, W. E. Renehan,

J. Neurophysiol. 64, 3 (1990).28. G. Pinganaud, I. Bernat, P. Buisseret, C. Buisseret-Delmas,

J. Comp. Neurol. 415, 91 (1999).29. D. N. Hill, R. Bermejo, H. P. Zeigler, D. Kleinfeld,

J. Neurosci. 28, 3438 (2008).30. J. D. Coulter, E. G. Jones, Brain Res. 129, 335 (1977).31. J. A. Rathelot, P. L. Strick, Proc. Natl. Acad. Sci. U.S.A.

103, 8257 (2006).32. W. I. Welker, R. M. Benjamin, R. C. Miles, C. N. Woolsey,

J. Neurophysiol. 20, 347 (1957).33. G. Paxinos, K. Franklin, The Mouse Brain in Stereotaxic

Coordinates (Academic Press, San Diego, CA, ed. 2, 2001).34. We thank H. Bokor and L. Acsady for advice on brainstem

anatomy and lesions and K. Svoboda (Addgene plasmid20071) and C. Lüscher (virus) for AAV-ChR2. This work wasfunded by grants from the Swiss National Science Foundation(C.C.H.P.), Human Frontiers in Science Program (C.C.H.P.),SystemsX.ch (C.C.H.P.), and a European Molecular BiologyOrganization long-term fellowship (F. Matyas).

Supporting Online Materialwww.sciencemag.org/cgi/content/full/330/6008/1240/DC1Materials and MethodsFigs. S1 to S4ReferencesMovies S1 and S2

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Fig. 4. Motor signaling pathways from S1 and M1. (A) Lentivirus-labeled axonalprojection into M1 by neurons located in the C2 barrel column of S1 (red).Biotinylated dextran amine (BDA)was injected into this region ofM1 (green). In theoverlay, colocalization appears in yellow. (B) The lentiviral injection site in S1 barrelfield (S1-BF) of the samemouse is strongly labeled alongwith the axonal projectionto S2 (red). The BDA-labeled axonal projections into S1 from M1 (green) arborizeprimarily in layers 1, 5, and 6 of the barrel field (S1-BF) and the surroundingdysgranular zone (S1-DZ). (C) M1 (green) projects to the brainstem reticular

formation (RF), and S1 (red) projects to spinal trigeminal nuclei (SP5) of the samemouse. Schematic drawing (left) adapted from Paxinos and Franklin (33). (D)Microstimulation of RF evoked whisker protraction, whereas microstimulation ofSP5 drove whisker retraction. Microstimulation locations were marked with lesions,and fixed sections were cytochrome oxidase stained. (E) Amplitudes and latenciesfor whiskermovement evoked bymicrostimulation of SP5 (n=4mice) and RF (n=3 mice) (mean T SD). (F) Schematic drawing of two parallel whisker motorpathways from the cortex to the motor neurons located in the facial nucleus (FN).

www.sciencemag.org SCIENCE VOL 330 26 NOVEMBER 2010 1243

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Motor Control by Sensory Cortex

Carl C. H. PetersenFerenc Matyas, Varun Sreenivasan, Fred Marbach, Catherine Wacongne, Boglarka Barsy, Celine Mateo, Rachel Aronoff and

DOI: 10.1126/science.1195797 (6008), 1240-1243.330Science 

repertoire useful for a mouse seeking food and shelter in a complex environment.cortex is also motor and the motor cortex is also sensory. In an ecological context, these combined reactions offer a command for retraction. Similarly, the motor cortex stimulates protraction for more active exploration. Hence, the sensorymovements (retraction) of whiskers. So if a whisker hits an object, then a reasonable first reaction might be a motor cortex controlled the forward movement (protraction) of their whiskers and the sensory cortex controlled backwardshave found that sensory and motor fields are specialized for different types of movement, such that in mice the motor

(p. 1240)et al.Matyas perceiving movement. However, in the real world, this may not always be so neatly arranged. Every student learns that the sensory cortex is used for processing sensation and the motor cortex is used for

By a Whisker

ARTICLE TOOLS http://science.sciencemag.org/content/330/6008/1240

MATERIALSSUPPLEMENTARY http://science.sciencemag.org/content/suppl/2010/11/22/330.6008.1240.DC1

REFERENCES

http://science.sciencemag.org/content/330/6008/1240#BIBLThis article cites 31 articles, 7 of which you can access for free

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is a registered trademark of AAAS.ScienceScience, 1200 New York Avenue NW, Washington, DC 20005. The title (print ISSN 0036-8075; online ISSN 1095-9203) is published by the American Association for the Advancement ofScience

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