0, p = 0.04) and higher order areas (t10 = 2.6, p = 0.01). Although we lacked coverage of early visual areas in the medial and posterior cortex, we observed a trend from midlevel visual areas in the ventral and dorsal stream toward larger TRWs in higher order visual areas. The TRW values from frontal cortical electrodes were higher than in all other ROIs buy FG-4592 (Figure 5B). Having found TRW patterns in ECoG that substantially match prior neuroimaging results (Hasson et al.,

2008; Lerner et al., 2011), we next tested the hypothesis that regions with longer TRWs should exhibit a shift toward a slower timescale of dynamics. We assessed the timescales of neuronal population dynamics using two metrics: first, a measure of low-frequency variance in the power time courses, and second, a measure of temporal autocorrelation in the power time courses. To measure the low-frequency variance in the power fluctuations, we first

calculated the “modulation spectrum” of each electrode: this is the power spectrum of the 64–200 Hz power fluctuations at each site. After dividing the electrodes via a median split on TRW values (median TRW value = 0.11), we averaged the modulation spectra within the “long TRW” and “short TRW” groups. The group of long TRW electrodes showed relatively more slow fluctuations than the group of short TRW electrodes (Figure 6A). The increase was most apparent below 0.1 Hz, and was seen in both the intact and fine-scrambled conditions. To quantify the strength of the slow fluctuations, we computed the fraction of the modulation spectrum that was below 0.1 Hz at each BLZ945 clinical trial site. We refer to this normalized about amplitude of slow fluctuations as “LowFq” (see Experimental Procedures; and also Zuo et al. [2010]). LowFq values range from 0 (indicating faster dynamics) to 1 (indicating slower dynamics). LowFq values were higher in the long TRW group

than in the group of short TRW electrodes (Figure 6B). This was evident for both the intact and fine-scrambled movie conditions. These observations were confirmed in a 2-way ANOVA with factors of stimulus (intact/fine-scrambled) and TRW (long/short): both factors significantly modulated LowFq (p < 0.01) but the interaction was not significant (p = 0.24). The fraction of slow fluctuations in power was also associated with TRWs on an electrode-by-electrode basis. LowFq values measured during the intact movie were robustly correlated across electrodes with TRW values (r = 0.46, p = 3e-5; Figure 6C). The same effect was observed when measuring LowFq in the fine-scrambled movie (r = 0.37, p = 0.001; Figure 6D). Partial correlations between LowFq and TRW values, with repeat reliability (rINTACT or rFINE) included as a covariate, were also highly significant (p < 0.01 all comparisons). This indicates that the relationship between LowFq and TRW was not due to a link between LowFq and electrode responsiveness within a single condition.

E.P. thanks the Philippe and Bettencourt-Schueller Foundations. A.C.L. and S.L. are supported by a Sir Henry Wellcome Postdoctoral Fellowship and an EMBO Long-Term Fellowship, respectively. S.W. is funded by a Wellcome Trust Senior Research Fellowship in the Basic Biomedical Sciences, grant MH081982 from the National Institutes Bortezomib cost of Health, and by funds from the Gatsby Charitable Foundation and Oxford Martin School. “
“While the physiological importance of electrical synaptic transmission

in cold-blooded vertebrates has long been established (Bennett, 1977), progress over the last decade has also revealed the widespread distribution of electrical synapses, and this modality of synaptic transmission was reported to underlie important functional processes in diverse regions of the mammalian CNS (Connors and Long, 2004). Consequently, electrical transmission is now considered an essential form of interneuronal communication that, together with chemical transmission, dynamically distributes the processing of information within neural networks. In contrast to detailed knowledge of the mechanisms underlying chemical transmission, far less is known about how the

molecular architecture or the potentially diverse biophysical properties of electrical synapses encountered in physiologically Pifithrin-�� disparate neural systems govern their function or impact on characteristics of electrical transmission Megestrol Acetate in those systems. Electrical synaptic transmission is mediated by clusters of intercellular channels that are assembled as gap junctions (GJs). Each intercellular channel is formed by the

docking of two hexameric connexin hemichannels (or connexons), which are individually contributed by each of the adjoining cells, forming molecular pathways for the direct transfer of signaling molecules and for the spread of electrical currents between cells. As a result, electrical synapses are often perceived as symmetrical structures, at which pre- and postsynaptic sites are viewed as the mirror image of each other. Connexons are formed by proteins called connexins that are the products of a multigene family that is unique to chordates (Cruciani and Mikalsen, 2007). Because of its widespread expression in neurons, connexin 36 (Cx36) is considered the main “synaptic” connexin in mammals. In contrast to other connexins, such as some found in glia (Yum et al., 2007 and Orthmann-Murphy et al., 2007), all pairing configurations tested so far indicate that Cx36 forms only “homotypic” intercellular channels (Teubner et al., 2000 and Li et al., 2004), where connexons composed of Cx36 pair only with apposing Cx36-containing connexons. Notably, the number of neuronal connexins is higher in teleost fishes, which, as a result of a genome duplication (Volff, 2005), have more than one homolog gene for most mammalian connexins (Eastman et al., 2006).

Après mon exposé Eccles m’a demandé où j’avais appris ça. Je lui répondis “nulle part, et j’ai tout fait moi-même”. Eccles a été très impressionné et m’a invité à venir à Canberra, tous frais payés. De retour à Kiev, j’ai préparé tous les documents nécessaires et les ai fait parvenir au service des relations internationales. Des semaines et des mois passèrent sans réponse. Je ne fis aucune démarche pour accélérer la décision de l’administration mais

un jour la direction reçut un appel téléphonique international, selleck ce qui était très rare à l’époque. C’était Eccles, qui voulait savoir pourquoi je n’étais pas venu à Canberra. Je lui répondis que la décision ne dépendait pas de moi. Eccles a très bien compris et a dit: “Très bien, je vais envoyer un télégramme à Khrouchtchev”. AZD6738 in vivo Bien sûr, cette communication téléphonique ne resta pas confidentielle, et suscita un grand émoi

dans l’institut. Je ne sais pas si Eccles a vraiment contacté N.S. Khrouchtchev mais, quoiqu’il en soit, je reçus tous les documents quelques jours après. C’est ainsi que je me suis rendu en Australie où j’ai travaillé pendant six mois». Lors de cette courte période P.G. Kostyuk noua de sérieuses relations avec un grand nombre de scientifiques de divers pays et ne publia pas moins de 5 articles scientifiques. L’hypothèse de Eccles-Kostyuk-Schmidt, formulée à la fin des années 60, sur l’existence de 2 systèmes de régulation présynaptique du signal nerveux est entrée dans tous les manuels de neurophysiologie et fut étudiée dans toutes les universités (Fig. 4). C’est à cette époque que P.G. Kostyuk a commencé à publier dans Non-specific serine/threonine protein kinase des journaux internationaux. En 1966, il fut nommé directeur de l’Institut de Physiologie Bogomolets qu’il dirigera pendant près de 45 ans. Sous sa direction, cet institut est devenu l’un des meilleurs centres de recherche en neurosciences non seulement en URSS mais aussi au niveau international.

Des chercheurs remarquables comme V. Skok, M. Shuba et O. Krishtal en sont issus. En 1979 grâce à l’énergie et l’autorité de Platon Kostyuk de nouveaux bâtiments ont été construits et équipés d’instruments modernes. Beaucoup de conférences, de congrès et d’enseignements scientifiques s’y sont déroulés, attirant de nombreux chercheurs du monde entier. Des collaborations étroites ont été nouées avec la plupart des Universités et des Instituts les plus prestigieux d’Europe comme des Etats-Unis d’Amérique ou du Japon. Des découvertes importantes y ont été réalisées. L’enregistrement des courants transmembranaires de cellules au contenu intracellulaire modifié par la méthode de perfusion intracellulaire, qu’il a mise au point, a permis de caractériser de nouveaux types de canaux ioniques.

“
“The authors regret that errors appeared in the Abstract and Materials and methods section. The corrected full sentences appear below (corrections in bold text): Page 347, Abstract, Line 3–5: Here the authors evaluated the effect of a combination of PCI-32765 order doxycycline (10 mg/kg/sid for 30 days) and ivermectin–pyrantel (6 μg/kg of ivermectin + 5 mg/kg of pyrantel every 15 days for 180 days) on microfilariemia, antigenemia and parasite load at echocardiography in naturally infected dogs from an endemic region of Italy.

Page 348, 2. Materials and methods, 2.1. Animals and methods, Lines 12–16: Enrolled dogs were treated with doxycycline (Ronaxan1, Merial) at 10 mg/kg daily for 30 days and with ivermectin–pyrantel pamoate (Cardotek Plus1, Merial) at a minimum dose of 6 μg/kg of ivermectin + 5 mg/kg of pyrantel once every 15 days for 6 months. “
“Tritrichomonas mobilensis is a common intestinal trichomonad of squirrel monkeys, such as Saimiri spp., which have been used in biomedical research ( Pindak

et al., 1985 and Culberson et al., 1986). The role of this parasite in gastrointestinal pathology of monkeys has not been well established. It has been demonstrated that T. mobilensis is invasive in natural hosts ( Scimeca et al., 1989) as well as in experimental animals ( Culberson et al., 1988); however, inflammatory check details response in the natural host of this parasite has not been observed. Newborn squirrel monkeys are free of this parasite but acquire it at 1–2 months of age either from their mothers or from cage mates ( Brady et al., 1988). Sampling of a large number of adults failed to identify trichomonad-free individuals during suggesting that squirrel monkeys may be life-long carriers of T. mobilensis ( Pindak et al., 1988). Tritrichomonas foetus is the causative agent of cattle trichomonosis, which is one of the most prevalent sexually transmitted disease in cattle. In cows, the infection varies from a mild vaginitis or cervicitis, to endometritis, abortion and infertility. Significant losses may occur because of infertility and abortion ( BonDurant, 2005). T. foetus is currently recognized as the agent of feline trichomonosis, which is a large bowel disease in domestic cats ( Tolbert

and Gookin, 2009). In literature from the 1990s and even more recently, a hypothesis has been raised suggesting that T. mobilensis, T. foetus and Tritrichomonas suis (a gastrointestinal commensal of pigs) are the same species ( Felleisen, 1997 and Kleina et al., 2004). These groups analyzed both the internal transcribed space (ITS) regions and 5.8S rRNA genes, and they claimed that T. foetus and T. suis had identical sequences and that only one substitution was found in the ITS2 region of T. mobilensis. However, Felleisen (1998) tested the randomly amplified polymorphic DNA from the same three species and reported that T. mobilensis was genetically distinct from the other tritrichomonads. Recently, further structural and molecular studies confirmed that T. foetus and T.

We then proceeded to the calcium imaging 30 min after the last session of the stay task to see whether the activity pattern was

the same as or different from that in the avoidance task. Even after fish learned the stay task, we continued to observe activation in the dorsal telencephalon. However, remarkably, the activated areas observed after the stay task appeared slightly, but significantly, different from that observed Vorinostat cost in the initial avoidance task. The activated area was extended in a lateral and posterior direction (Figure 5C). The observed activity pattern difference was not the consequence of repeating conditioning in 2 consecutive days, because fish that were trained by the avoidance task on the first day and then by the avoidance task again on the next day showed calcium activity patterns similar to those observed 24 hr after the three avoidance conditioning

sessions were given and were not repeated any more (Figure S5C). In order to examine whether the enlargement did not appear simply because of the passage of time, we gave the fish Enzalutamide manufacturer only cues without punishment on the next day of the initial avoidance task. Even after four sessions, the acquired avoidance behavior was not extinguished (Figure S5D3). Consistent with the behavioral result, the calcium activity pattern in these fish was relatively similar to but did not get larger than that observed at 24 hr after the avoidance conditioning, further supporting the idea that the enlarged calcium activity pattern for the stay

task is specific to the learned stay behavior (Figures S5D1 and S5D2). When the centers of the activated areas for individual fish were collectively plotted with respect to standardized STK38 anatomical landmarks of the telencephalon (see Experimental Procedures), the clusters of activity centers between the avoidance task- and stay task-trained groups demonstrated a significantly different spatial pattern (Figure 5D). Importantly, the distances from the average point for the avoidance task (Figure 5D, orange crosses) to each activity center for the stay task were significantly larger than those to each activity center for the avoidance task in both hemispheres (Figure 5E1). Likewise, the distances from the average point for the stay task (Figure 5D, green crosses) to each activity center for the avoidance task were significantly larger than those to each activity center for the stay task in both hemispheres (Figure 5E2). These analyses indicate that the patterns of clustered activity were significantly shifted between the avoidance and stay tasks. We compared the time sequence of stay and avoidance activity and found no significant difference of the peak time (Figures S5B1, S5B2, and S5G, left telencephalon, p = 0.0931, unpaired t test; right telencephalon, p = 0.0599, unpaired t test).

Our findings implicate an excitatory neural population in the generation of rhythmicity. We note that the activity of inhibitory neurons involved in reciprocal inhibition between rhythm-generating centers could also influence the frequency of the motor rhythm. Decreasing inhibition in such populations of inhibitory neurons will phase-delay the switching between half-centers, thereby decreasing the frequency of the locomotor rhythm. This effect is most likely what is observed after ablation of inhibitory En1+ neurons (Gosgnach et al., 2006) suggesting that at least part of this population is responsible for reciprocal inhibition

between rhythm-generating half-centers. In addition to connectivity between Shox2 INs, some Shox2 INs provide direct excitation to commissural neurons. Although we show that Shox2off V2a neurons are necessary for normal left-right alternation (see above and Figure 8A), these are not marked by GFP in the Shox2::Cre; Z/EG. Therefore, Metabolism inhibitor these findings demonstrate that Shox2+ V2a and/or Shox2+ non-V2a INs also project to commissural pathways. We speculate

that Shox2+ non-V2a neurons are likely candidates for these projections. So why is left-right coordination not affected in the Shox2–vGluT2Δ/Δ or Shox2-eNpHR mice? The most selleckchem likely explanation for this is that the Shox2+ non-V2a INs and the Shox2off V2a INs drive commissural pathways active at different speeds of locomotion ( Figure 8B; see also Talpalar et al., 2013). The Shox2off V2a commissural pathway seems to be active at medium to high speeds ( Crone et al., 2009) and it is likely that non-V2a Shox2+ neurons, together with other yet-to-be-identified iEINs, drive left-right alternation at lower frequencies of locomotion. Therefore, left-right alternation

at higher frequencies is supported by Shox2off V2a INs and at lower speeds the other rhythm-generating iEINs are capable of maintaining left-right alternation ( Figure 8B). Transsynaptic virus injections demonstrate that many Shox2 INs are premotor INs and located in a lateral population within the spinal cord. Our findings that ablating Shox2+ V2a neurons in the Shox2-Chx10DTA mice does not affect the locomotor frequency Adenosine but leads to increased variability of locomotor bursts strongly suggests that locomotor-related premotor Shox2 INs are Shox2+ V2a neurons. These Shox2+ V2a neurons would then be downstream of the rhythm-generating kernel (Figure 8B). Flexor dominance was detected both in the firing of rhythmic Shox2 INs as well as connectivity profile analysis to motor neurons. In a comparative analysis, we detected approximately three times more Shox2 INs connecting to flexor (TA) than to extensor (GS) motor neurons. This observation is in line with previous findings showing that premotor neurons provide a much stronger synaptic excitation to flexor motor neurons than to extensor motor neurons during locomotor-like activity (Endo and Kiehn, 2008).

g., permethrin, deltamethrin, flumethrin), selamectin (macrocyclic lactone), or spinosad (spinosyns). A huge range of strategies have been used in this bloody combat, by applying these acaricides and insecticides topically as sprays, dips, spot-on, collars, showers, or more recently orally, with different treatment regimes. The battle against ticks is almost entirely Obeticholic Acid nmr focussed to enhance the speed of kill (which may ultimately led to prevents VBD infections) and the residual activity of these weapons, with good acaricidal products characterized by >90% efficacy reached within 48 h post-treatment and

by the ability to prevent re-infestations. On the other hand, the optimal control of fleas aim not only to eliminate adults on the host and to prevent their re-infestation, but also to “clean” the environment contaminated by eggs, larvae and pupae with appropriate levels of residual activity. However, in this never-ending duel to protect dogs from ectoparasites, the choice of the chemical compounds available on the market is pivotal for increasing the chances of success. This is also

vital for reducing the risk that enemies survive previous compounds, thus offering a AZD9291 in vivo higher “resistance” against them. Therefore, in spite of the abundance of molecules developed by leader companies in the field, there is an increasing request for new molecules against ticks and fleas. This Special Edition of Veterinary Parasitology represents a collection of selected papers describing a new antiparasitic drug that veterinarians and pet owners have from today onwards to control ticks and fleas on dogs. This product contains afoxolaner, a novel ectoparasiticide administered orally in a chewable formulation (NEXGARD® Merial) to treat and control flea and tick infestations in dogs, for one month following a single administration. This compound is a member of the isoxazoline family, which works by inhibiting insect GABA and Glutamate-gated chloride channels, binding to a site distinct from that of existing insecticidal molecules. Beyond the mode of action,

the ease of its utilization and its systemic distribution represent strong features of this product, which will soon be available on the market for the prevention and cure of ticks others and fleas. The product has been formulated for preventing and cure infestation by fleas (Ctenocephalides felis felis and Ctenocephalides canis) and ticks (Dermacentor reticulatus, Dermacentor variabilis, Haemaphysalis longicornis, Ixodes ricinus, Ixodes scapularis, Rhipicephalus sanguineus sensu lato) for at least 5 and 4 weeks, respectively. The complete speed of kill for fleas is obtained in 8 h, with elimination of new flea infestations within 12 h. As far as ticks, they are killed within 48 h after infestation therefore reducing the possibility for pathogen transmission.

, 1966 and Suga, 1968). Along the central auditory pathway of rats, such neurons have been observed in the inferior colliculus (Clopton and Winfield, 1974, Selleck HKI-272 Felsheim and Ostwald, 1996 and Rees and Møller, 1983), the medial geniculate body (Lui and Mendelson, 2003), and

the auditory cortex (Ricketts et al., 1998, Ye et al., 2010 and Zhang et al., 2003). Direction selectivity (DS) of cortical neurons is inherited from their excitatory inputs and shaped by cortical inhibition, and its topography is highly correlated with the tonotopic map (Zhang et al., 2003). Because the selectivity for FM direction is not observed in the auditory nerve fibers (Sinex and Geisler, 1981), the inputs to the central auditory system, it is reasonable to assume that direction selectivity and its topography emerges somewhere between the cochlear nuclei and the auditory cortex. Previous studies suggest that the inferior colliculus is the major processing stage at which direction selectivity is constructed, because PLX-4720 order most of the cells in lower auditory nuclei are not direction selective, especially in rats (Moller, 1969 and Poon et al., 1992). Two mechanisms are hypothesized to explain the emergence of direction selectivity (Gittelman et al., 2009 and Suga, 1968). One hypothesis relies on the temporal asymmetry between excitation and

inhibition, in which the preferred direction activates excitatory inputs first, whereas the null direction activates inhibitory inputs first. The second hypothesis depends on the temporal coincidence of the arrival of the synaptic inputs, in which the preferred direction activates more coincident excitatory inputs or less coincident Terminal deoxynucleotidyl transferase inhibitory inputs, whereas the situation is reversed for the null direction. It is worth noting that to prove either hypothesis requires a clear dissection of synaptic inputs to the identified DS neurons. Recently, several studies suggested that inhibition shapes neurons’ direction selectivity, which is inherited from presynaptic neurons at different

processing stages (Gittelman et al., 2009, Ye et al., 2010 and Zhang et al., 2003). However, to understand the synaptic circuitry mechanisms that generate direction-selective responses, we have to target those DS neurons receiving nonselective inputs and directly examine both their excitatory and inhibitory inputs in sufficient detail. In this study, by using multiunit recording techniques, we mapped all the three major subcortical nuclei of the central auditory pathway, including the cochlear nuclei (CN), the inferior colliculus (IC), and the medial geniculate body (MGB) of rats, to search for DS neurons and their topography. With cell-attached (loose-patch) recordings followed by juxtacellular labeling, we identified the morphology of DS neurons in the IC post hoc.

, 2009, Rossignol and Ruxolitinib Dubuc, 1994 and Thompson et al., 2011). Raphespinal axons arise from cells in the midline raphe

(Figure 6) and travel caudally through the spinal cord as dispersed bundles of axons neighboring the central gray matter (Figure 6). Complete lesions of raphespinal axons require extensive bilateral lesions that extend ventrally well below the central canal. Accordingly, the most reliable model for examining regeneration of this system is a complete spinal cord transection or crush (Figure 6C). While there has been some question regarding the existence of intrinsic serotonin-containing neurons with the spinal cord that would complicate the assessment of axonal regeneration even below a complete transection site, routine serotonin immunohistochemistry with an antibody to 5-hydroxytyptamine (5HT) does not detect residual neuronal or axonal labeling below a complete injury (Figure 6C). Although there are few reports of regeneration after complete lesions (Coumans et al.,

2001), the extent of regeneration reported is modest. Many previous studies report treatment-related increases in serotonergic axons below an injury and growth of serotonergic axons into partial spinal cord lesion sites containing cell grafts (Lu et al., 2003). Such growth could result either from regeneration of transected axons or sprouting of neighboring axon terminals that were spared by the lesion. Distinguishing between Dasatinib in vivo these is probably impossible, so “increase in serotonergic axon density” or not “axon growth into the lesion site” is the most appropriate phrases for describing these forms of axon growth. Rubrospinal projections are considered to be rudimentary in humans although this point is not entirely settled (Nathan and Smith, 1982 and ten Donkelaar, 1988). In rodents, rubrospinal axons arise from the magnocellular division of the red nucleus (Figure 7A), cross the midline, and project through the dorsal part of the lateral column of the spinal cord and modulate motor function. (Küchler et al., 2002 and Morris

et al., 2011). Rubrospinal axons can be labeled by making tracer injections into the brainstem (Figures 7D and 7E show the pathway after injections in a mouse). The rubrospinal tract can be completely transected by lateral funicular lesions, which therefore represent an attractive model system for the study of mechanisms underlying motor axon regeneration, albeit with the important caveat that the projection is of limited importance in humans. Rubrospinal axons exhibit a greater capacity to regenerate than CST axons (Liu et al., 1999). This system, like others, is also subject to the caveat that growth into or beyond a lesion site can arise from either sprouting of spared axons or regeneration of transected axons unless it can be confirmed by complete reconstruction of axons extending past the lesion that growth originated from an axon that was unequivocally cut.

Wild-type

mice injected with H129ΔTK-TT showed no tdT expression in virally infected cells (identified by HSV-1 antigen expression; Figure 2B) as assessed both by native fluorescence and by anti-dsRED antibody staining (data not shown), indicating minimal leakage from the loxP-STOP-loxP cassette (Zinyk et al., 1998). We next examined labeling of cerebellar circuitry downstream of Purkinje cells in these mice. Purkinje cells axons, which are the main efferents from the cerebellar cortex, target the deep cerebellar nuclei (DCN). In H129ΔTK-TT infected Veliparib order mice, tdT could be detected in most of the three major subdivisions of the DCN—the fastigial nuclei (FN), the interposed nuclei (IP), and the dentate nucleus (DN) (Figures 2D–2F). We also detected labeling in known DCN targets (Ito, 1984), including the vestibular nuclei (VE; Figures 2G–2I), the inferior olive (IO; Figures 2J–2L), ventral lateral thalamus (VL; Figures 2M–2O), and the red nucleus (RN; Figures S1M–S1O).

Labeling was also observed in the interpeduncular nuclei, a target of fastigial axons (Snider et al., 1976) (Figures S1G–S1I), and in the hippocampus and cortical amygdala (Figures S1J–S1L). tdT labeling in all these structures was present in cell somata, as determined by counterstaining Galunisertib price with fluorescent Nissl (Figures 1F, 1I, 1L, and 1O). We determined the neuronal versus glial identity of these cells by costaining with antibody markers. In the inferior olive (IO), the majority of tdT expressing cells coexpressed the panneuronal marker NeuN (333/395; 85%), while only a very small percentage (1/45; 2%) coexpressed GFAP (Figures 2P–2R and Figures S2A–S2H). Qualitatively similar results were observed in the area postrema (AP) and nucleus of the solitary tract (NTS), two additional sites where anterograde labeling from infected Purkinje cells was

detected (Ross et al., 1981), and in the VPL (Figures S2I–S2X and Table S1). These data indicate oxyclozanide that the majority of tdT expressing cells labeled in the cerebellar pathway by H129ΔTK-TT virus are neurons. Unexpectedly, we observed tdT labeling in DBH+ neurons within the locus coeruleus (LC) (Figures S1A–S1C), which are known to project to Purkinje cells (Hoffer et al., 1973). Such LC labeling was not reported in previous transsynaptic labeling studies using wheat germ agglutinin (WGA) expressed from the same PCP/L7 promoter element, either in AAV (Braz et al., 2002) or in transgenic mice (Yoshihara, 2002 and Yoshihara et al., 1999). This labeling could therefore reflect retrograde transport of recombined virus released from infected Purkinje cells. However, we found that tdT-positive LC neurons ectopically expressed the cointegrated L7/PCP2-GFP/Cre transgene (Figures S1D–S1F and data not shown).