In the other set of trials, the orientation of the stimulus was task relevant, and the color had to be ignored. A vertical stimulus was associated with an eye movement to the right and a horizontal stimulus with a saccade to the left. The key point is that the visual stimuli do not uniquely determine

the response required to obtain the reward—the monkeys needed to understand and apply the rules to pick the correct response. While the monkeys were performing this task, neuronal spike activity and local field potentials (LFPs), which reflect rhythmic activity in small populations around the electrode tip, were recorded from dorsolateral PFC. To quantify neural synchrony, Buschman et al. (2012) computed coherence among pairs of LFP recordings. In B-Raf assay addition, the degree of coupling between individual cells and the LFP was quantified by computing spike-field synchrony. Interestingly, LFP coherence showed rule-specific Venetoclax datasheet effects in two different frequency ranges: the beta and the alpha band (Figure 1B). While beta-band effects (around 20–30 Hz) occurred immediately after stimulus onset, alpha-band coherence changes (around 10 Hz) were maximal after presentation of the cue signaling the current rule. This suggests that the observed coherence changes were associated with rule selection. For most electrode pairs, beta-band LFP coherence was rule specific (i.e., stronger for either the orientation

or the color rule). Based on this, two assemblies could be identified: color and orientation (Figure 1B). For each assembly, beta-band synchrony increased in trials in which the rule preferred by the neurons was applied. Interestingly, these two assemblies were not completely PTPRJ disjunct; there were local populations that could couple, albeit with different strength, into either assembly. In agreement, analysis of spike-field synchrony showed that the strength of coupling of individual cells

into these two assemblies depended on the rule that applied. Thus, beta-band coupling of orientation-preferring cells to the LFP of the orientation assembly was stronger in orientation rule trials compared to color rule trials. Buschman et al. (2012) conclude that rule-specific beta-band coupling can dynamically link neurons involved in processing the same rule. Enhanced beta-band synchrony may then be relevant for dynamically selecting the assembly that is currently task relevant. Interestingly, orientation-specific cells showed higher alpha coherence when a switch to the color rule occurred, but color rule-specific cells did not increase alpha coherence during switches to the orientation rule (Figure 1B). Based on reaction times, the orientation rule was easier to apply for the animals and they had greater difficulty switching away from it, indicating behavioral dominance of the stimulus orientation. Buschman et al.

Therefore the choice-aligned excitation was not caused by these later sensory events. To analyze the choice-aligned

excitation, we used a time window (gray area in Figure 6B) that does not contain the timing of the chosen feedback or reward delivery. The choice-aligned excitation increased as the search array size increased. This was statistically shown by a significant positive correlation between the magnitude of the excitation and the search array size in the DMS task (large reward trials, p < 0.01; small reward trials, p < 0.01; Wilcoxon signed-rank test) (Figure 6C). Comparing the correlation coefficients in the two tasks for each neuron (Figure 6D), the correlation was significantly greater in the DMS task than in the control Selleckchem AZD2281 task, especially for the large reward trials (large reward trials, p < 0.01; small reward trials, p > 0.05; Wilcoxon signed-rank this website test). These data suggest that the choice-aligned excitation was enhanced when the monkey found a correct target in the difficult search condition and when the large reward was expected. The choice-aligned excitation was observed even in error choice trials in which the monkey chose a wrong object (i.e., nontarget distracter) (Figure 7A). The averaged activity was aligned by the onset of the choice behavior in which the monkey

chose a wrong object in the six-size array condition. The magnitude of this excitation was significantly larger than zero in both the large reward trials (mean ± SD = 1.4 ± 4.1 spikes/s, p < 0.01, Wilcoxon signed-rank test) and the small reward trials (mean ± SD = 2.0 ± 4.5 spikes/s, p < 0.01, Wilcoxon signed-rank test). Thus, these neurons would be excited when the monkey identified an object as a correct target, even if it was not actually the correct target. Consistent with this idea, no excitation was observed when the monkey temporarily looked at a nontarget distracter and subsequently Phosphoprotein phosphatase changed his gaze to choose

another object (Figure 7B). The averaged activity was aligned by the time when monkey’s eye position entered into a nontarget window (distractor window), subsequently stayed in the window for more than 100 ms, and then went to another window. The averaged activity is shown for two cases: one for the last eye entrance before final choice (Figure 7B, right), and one for the second last eye entrance before final choice (Figure 7B, left). In either case, significant excitation or inhibition was not observed (last before final choice, large reward trials, mean ± SD = 0.4 ± 2.2 spikes/s, p > 0.05, small reward trials, mean ± SD = −0.2 ± 2.6 spikes/s, p > 0.05; second last before final choice, large reward trials, mean ± SD = 0.0 ± 3.7 spikes/s, p > 0.05, small reward trials, mean ± SD = −0.3 ± 2.8 spikes/s, p > 0.05; Wilcoxon signed-rank test).

, 1995). The asymptomatic form represents 20–40% of the serum-positive population, of which 80% actually develops the disease (Noli, 1999). In the Brazil in urban area of the northeast region, the asymptomatic form represent 30% of the serum positive population (Queiroz et al., 2009). The suppression of cellular immunity is the most important aspect in the pathogenesis and progression of canine disease. The absence of T cell response to antigens of Leishmania sp. is observed in vivo, with a negative leishmanin skin test ( Dos Santos et al., 2008). In dogs infected with Leishmania infantum, a reduction in the number selleck chemical of T lymphocytes in PBMC occurs ( Bourdoiseau et al., 1997) and disorganization of white pulp

in spleen tissue has been previously described ( Santana et al., 2008), but the mechanisms that are responsible for these changes have not yet been elucidated. In human acute infection, the reduction in T lymphocytes and mononuclear cells of peripheral blood and failure in immunity has been associated with apoptosis (Potestio et al., 2004). In mice experimentally infected with Leishmania see more donovani, an increase in the level

of spontaneous apoptosis in the spleen and liver compared to noninfected mice was also observed ( Alexander et al., 2001). In vitro findings also suggest the involvement of apoptosis in the mechanism of suppression observed in visceral leishmaniasis, the infection of macrophages by L. donovani increased the level of FAS in the membrane and sFASL in the culture supernatant, a mechanism that may contribute to increased sensitivity to apoptosis for T cells specific for Leishmania sp. ( Eidsmo et al., 2002). To investigate whether apoptosis is involved in the reduction in lymphocytes in peripheral blood and alterations in white pulp, apoptosis was quantified in dogs naturally infected

with L. (L.) chagasi presenting clinical manifestations and the structural disorganization in white pulp was correlated with the percentage of apoptosis in T cells. If proven, such findings could Resminostat contribute to improving our present understanding of the immunopathogenesis in infected dogs. The county of Araçatuba (21°12′32″ S; 50°25′38″ W), with an area of 1,167,311 km2, is located in the state of São Paulo, Brazil. It is a region known to be endemic for canine VL. This study was approved by the institutional Ethics and Animal Welfare Committee (Comissão de Ética em Experimentação Animal, CEEA, UNESP, process number 02232). A total of 13 adult dogs were used, males and females, aged between 2 and 4 years-old, of undefined breed and different weights, from the Zoonosis Control Center of Araçatuba (CCZA). The dogs were symptomatic and showing at least three clinical signs of canine VL. These could include fever, dermatitis, lymphoadenopathy, onychogryphosis, weight loss, cachexia, locomotor abnormalities, conjunctivitis, epistaxis, hepatosplenomegaly, edema, and apathy.

In the CVT, partial cross-protection against anal infection at study exit Enzalutamide in vitro was also observed in a combined analysis of HPV31, 33, or 45, for example 49.4% (95% CI: 30.3–63.6) in the full cohort [28]. Interestingly, while cross-protection against cervical infection by non-vaccine types was clearly observed in CVT women receiving three doses of Cervarix®, there was no indication

of cross-protection in those receiving two doses [27]. For instance, efficacy in the ATP cohort against 12 month persistent infection with HPV31, 33, and 45 combined was 41.3% (95% CI: 18.9–57.9) in women receiving three doses and -25.9% (95% CI: -334–66.1) in those receiving two doses. There were too few non-vaccine type infections in the women receiving one dose to meaningfully evaluate cross-protection in this group. Evidence from a Libraries long-term follow-up of a phase IIb trial of Cervarix® suggests that cross-protection might preferentially wane over time [31]. Protection from incident HPV16/18 infection remained consistently high (>90%) throughout the 6.4 years of follow-up, with a cumulative efficacy of 95.3% (95% CI: 87.3–99.6). In contrast, protection from HPV31 and HPV45 infection was 100% through the first 3 years, but then incident infections began to appear over the next 3 years, yielding cumulative efficacies of 59.8% see more (95% CI: 20.5–80.7)

and 77.7% (95% CI: 39.3–93.4) for HPV31 and HPV45, respectively. It will be important to evaluate in long-term field studies the public health impact of cross-protection afforded by the two vaccines. Evaluating cross-protection against disease endpoints is complicated by the fact that many

women with cervical disease are infected with more than one HPV type. Causal inferences can be made by determining the specific type(s) in a lesion biopsy or by assuming that the preceding most persistent infection is responsible for the CIN, but these approaches have limitations. Complicating the issue Rebamipide is the fact that infections by HPV16 and 18, the vaccine types, tend to progress to CIN more rapidly than infections by other high-risk types [22]. Thus, in a 4-year trial, the probability that the lesion in a co-infected woman will be due to the non-vaccine type is less than the probability that it will be due to a vaccine type. A conservative approach used in the PATRICIA trial to address this issue was to evaluate cross-protection after excluding cases that were co-infected with vaccine types [30]. This exclusion consistently results in lower efficacy estimates against non-vaccines type-associated lesions. For instance, for the composite endpoint of CIN2+ associated with any of 12 non-vaccine types, efficacy in the TVC-naïve cohort was 56.2% (95% CI: 37.2–65.0) if HPV16/18 co-infections were included and a non-significant 17.1% (95% CI: -25.5–45.4) if HPV16/18 co-infections were excluded. However, the corresponding efficacies against CIN3+ were significant in both cases, 91.4% (95% CI: 65.0–99.0) and 81.9% (95% CI: 17.1–98.1), respectively.

All animals in this study were 4 months old at the time of inoculation. Sheep

(Suffolk cross, Rideau Arcott cross, Ile-de-France cross with Rideau Arcott) and goats (Alpine-Boer cross) were obtained from breeders in Manitoba. All animal manipulations were approved by the Animal Care Committee of the Canadian Libraries Science Centre for Human and Animal Health in compliance with the Canadian Council on Animal Care guidelines (Animal Use Documents #C-08-007, #C-09-004, #C-10-001, #C-11-011). The work with infected animals was performed under containment level 3 conditions (zoonotic BSL-3 Ag). Animals were acclimatized for two weeks prior to inoculation and inoculated subcutaneously MI-773 in vivo (SC) with 1 ml of RVFV (ZH501) into the right side of the neck, and if applicable re-inoculated SC or intravenously (IV) depending on the inoculation group. Two doses were compared: “low” dose of 105 PFU per animal and “high” dose of 107 PFU per animal. Rectal temperatures were taken for three days following arrival of the animal to the facility

and for minimum of five days prior to inoculation, Kinase Inhibitor Library cost and daily during the first week post inoculation. Except for the first group (sheep group A; see below), blood was collected daily for up to 6 or 7 days post inoculation (dpi). At this time point animals were either euthanized to determine virus presence in liver and spleen, or were kept up to 35 dpi for serum production, and bled weekly to follow antibody development (not reported in this manuscript). Overview of the inoculation groups is provided in Table 1. Where it was possible to group animals to compare two experimental

approaches, Student’s t-test was performed. A P value <0.05 was considered statistically significant. Sheep: Group S-A: eight animals (Suffolk cross) were inoculated with 105 PFU of RVFV prepared in Vero E6 cells. In this pilot trial, blood was collected at 3, 5 and 7 dpi. Group S-B: four animals (Rideau Arcott cross) were inoculated with 105 PFU of RVFV Vero E6 stock. Group S-C: four animals (Rideau Arcott cross) were inoculated with 105 PFU of RVFV C6/36-stock. Group S-D: four animals (Rideau Arcott Dipeptidyl peptidase cross) were inoculated with 107 PFU of Vero E6 stock. Group S-E: eight animals (Rideau Arcott cross) were inoculated with 107 PFU of C6/36-stock in two separate trials. Group S-F: four animals (Rideau Arcott cross) were inoculated with 107 PFU of C6/36 stock and re-inoculated at 1 dpi SC with the same dose. Group S-G: 4 animals (Rideau cross with Arcott or Ile de France) were inoculated with 107 PFU of the C6/36 derived virus stock, followed by IV inoculation with the same dose at 1 dpi. Most of the sheep were euthanized at 6–7 dpi, except for few animals kept for antibody production for 28 dpi. Some of the animals kept for production of antiserum were boosted at 14 dpi. Goats: All animals were Boer cross in groups of four. Group G-A was inoculated with 105 PFU of Vero E6 derived RVFV stock. Group B G-B was inoculated with 105 PFU of C6/36 derived RVFV stock.

Decisions and recommendations taken by the committee enjoy the highest level of credibility among the various bodies concerned, including the Ministry of Health, non-health government ministries and the private sector. The official terms of reference Selleck Erlotinib for the committee include: advising on the technical specifications for vaccines; advising on the standards and regulations for prescribing, providing, transporting and storing vaccines, both in the public and private health sectors; advising on the documents

and types of data to be collected on adverse events; and taking measures to avoid preventable, adverse events. They also specify that the committee advise on the significance of epidemiological or clinical studies submitted in support of these vaccines at their registration and thereafter, recommending policies for regulating the use of these vaccines in the Sultanate. The scope of the committee’s activities extends to vaccines and immunization as well as to other infectious diseases. It addresses these issues Modulators within the parameters of the Terms of Reference. Within Birinapant in vitro the area of vaccines and immunization, the committee decides on the use of new vaccines,

most recently the seven-valent pneumococcal conjugate vaccine (PCV-7), the inactivated poliovirus vaccine (IPV) and the Haemophilus influenzae type b conjugate-hepatitis-B-DTwP (pentavalent) vaccine. It has also recommended vaccination schedules for these vaccines and has furthermore made recommendations on vaccines for high-risk groups, including targeted immunization against seasonal influenza, meningococcal meningitis and rubella. Different formulations for the pentavalent vaccine have been considered, as have vaccines extending beyond infant schedules to all vaccine-preventable diseases. Finally, the committee has made recommendations on specific vaccines, commissioning to outside experts impact studies on hepatitis-B vaccination as well as

cost-effectiveness studies on the rotavirus and PCV-7 vaccines. Minutes of committee meetings and a record Dichloromethane dehalogenase of their recommendations are summarized and publicized on a regular basis in a national newsletter distributed to all health sector professionals, including physicians, members of the Ministry of Health and university researchers. The meetings themselves are closed. Committee members are appointed for a period of 3 years by the Minister of Health and may be re-appointed thereafter for another 3 years maximum. These appointments are made on the basis of nominations given by the Director General for Health Affairs (DGHA), the Director of the Department of Communicable Disease Surveillance and Control (DCDSC), the Chair and other committee members. There are also four ex officio members on the committee. They participate in the discussions that lead to the required consensus.

Additional in vitro studies in slice preparations suggested that the SWS-induced potentiation of cortical responses is mediated by a calcium-dependent postsynaptic mechanism that requires coactivation learn more of AMPA and NMDA receptors, further corroborating the view of synaptic potentiation rather than downscaling induced by SWS. While the synaptic homeostasis hypothesis allocates such long-term potentiation (LTP)-mediated synaptic upscaling to the waking brain, neither in vivo nor in vitro recordings by Chauvette et al. revealed any hints that cortical responsiveness globally increases across the wake period. Interestingly, the upscaling of excitatory postsynaptic

potential responses observed after SWS-like stimulation patterns in vitro occurred only when the stimulation pattern included an intracellular hyperpolarizing current pulse mimicking the down phase of the slow waves. While the hyperpolarizing down phase of a slow wave has been considered a time framing signal resetting activity in extended cortical networks (e.g., Mölle and Born, 2011), this result is the first to indicate a functional significance specifically for the slow-wave down state for LTP. In showing that the slow waves of SWS can convey LTP-mediated synaptic upscaling, Chauvette et al.’s findings provide a neurophysiological basis for a rapidly growing body of

data indicating a particular role for SWS in memory consolidation (Diekelmann and Born, 2010). Cortical representations, corticostriatal representations, and episodic memory representations

extending over hippocampo-neocortical networks all appear to be enhanced by SWS (e.g., selleck kinase inhibitor Frank et al., 2001; Huber et al., 2004; Wilhelm et al., 2011), and a causal contribution of slow oscillations (∼0.75 Hz) has also been demonstrated (Marshall et al., 2006). Processes of sleep-dependent memory enhancement in these studies Phosphoprotein phosphatase could well incur the net upscaling of cortical networks mediated by postlearning SWS. However, Chauvette et al.’s findings appear to contradict the body of evidence arguing toward synaptic downscaling across sleep. For example, by measuring miniature excitatory postsynaptic currents, a valid indicator of synaptic scaling, Liu et al. (2010) showed signs of increased synaptic potentiation at the end of the wake period and reduced potentiation after sleep in rodent frontal cortex slices. Also, Vyazovskiy et al. (2008) showed that the slope and amplitude of cortical evoked responses to electrical stimulation were increased after wakefulness and decreased after sleep, with these changes correlating with changes in slow-wave activity. Moreover, amplitude and slope of slow waves, as well as the synchrony of cortical cell firing with slow waves, were found to decrease across periods of SWS (Vyazovskiy et al., 2009). Collectively, these and many other studies provide compelling evidence that there are global processes of synaptic downscaling at work during sleep.

OBP49a was purified by serial use of HiTrap SP XL 5 ml and HiTrap Q XL 5 ml columns (GE Healthcare), followed click here by affinity purification with OBP49a antibodies. The purity of OBP49a was assessed by fractionation of the protein by SDS-PAGE and silver staining ( Figures S4C and S4D). SPR was conducted using a BIAcore 3000 (GE Healthcare)

at 25°C. Coupling of OBP49a to CM5 chips (GE Healthcare) was performed by injecting 0.1 μg/ml of protein with 10 mM sodium acetate, pH 4.0, at a 5 μl/min flow rate, and confirmed by an increase of 10,000 resonance units on the sensor chip. The chemicals were diluted to the indicated concentrations in continuous flow buffer (HBS-P [10 mM HEPES pH 7.4, 150 mM NaCl, 0.005% Surfactant P20]). Each analytic run was performed at a 30 μl/min flow rate. The chip matrix was regenerated using 20 mM NaOH after each binding analysis. To obtain the UAS-YFP(1):Gr64a, UAS-YFP(1):Gr64f transgenic flies for the PCA, we first generated pUAST-YFP(1) by PCR amplifying a 462 bp YFP(1) www.selleckchem.com/products/3-methyladenine.html fragment from pAKAR3EV ( Komatsu et al., 2011) that extended from the Kozak sequence. This fragment was subcloned between the EcoRI and KpnI sites of pUAST. We then inserted

the coding sequences of Gr64a and Gr64f into pUAST-YFP(1), so that YFP(1) was linked to the N termini of the GRs. To produce the pUAST-OBP49a-t-YFP(2) construct, we used pUAST-Obp49a-t to PCR amplify the OBP49a-t coding sequence that lacked the stop codon, and then inserted the fragment into pUAST. We then used pAKAR3EV as the template to PCR amplify two DNA fragments encoding a 116 amino acid long flexible EV linker and YFP(2), which encoded residues 155–237 of YFP. We inserted these DNA fragments adjacent to the 3′ end of the OBP49a-t coding region. We expressed these transgenes, as well as UAS-Snmp1-YFP(2) ( Benton et al., almost 2007), under the control of Gr5a-GAL4. To apply berberine to the sensilla, we immobilized the flies with a glass capillary and dipped the labella

into a solution containing 100 μM berberine for 1 min before dissecting the labella. We also immersed labella in 100 μM berberine/100 mM sucrose solutions, and obtained results indistinguishable from those generated with untreated labella or labella dipped in berberine only (data not shown). The labella were fixed with 4% paraformaldehyde in PBS-T (0.2% Triton X-100 in PBS) for 20 min. Fixed labella were washed with PBS-T three times, cut in half with a razor blade, and then mounted in VECTASHIELD (Vector Laboratories). Fluorescence was viewed in whole mounts of labella using a Zeiss LSM700 confocal microscope. All error bars represent SEMs. Unpaired Student’s t tests were used to compare two sets of data. ANOVA with Tukey post hoc tests were used to compare multiple sets of data. Asterisks indicate statistical significance (∗p < 0.05, ∗∗p < 0.01). We thank FlyBase, the Bloomington Stock Center and Drs. K. Scott, L. Vosshall, J.W. Posakony, and Y.D. Chung for fly stocks, and Dr. C.Y. Park and Mr. J.

Despite the research conducted concerning the principal component structure of vertical jumping in male athletes, no studies addressing this issue in female athletes have been found. It is well documented that vertical jumping performance is significantly different between males and females due to the existing gender differences concerning the strength and power production abilities.27, 28 and 29 Furthermore, it has been reported

that although the temporal parameters are not different, significant gender differences exist concerning the magnitude of the force dominancy of maximal vertical squat jump (SQJ) performance Z-VAD-FMK concentration in untrained young adult males and females.30 Since previous studies have reported differences concerning the principal component structure of vertical jumping only for male athletes of various sport-specific backgrounds,22, 23, 24, 25 and 26 it is of interest to examine the effect of sport specificity on the maximal SQJ performance indices in female athletes. The purpose of the present study was to investigate the possibility that young adult female athletes from different sports utilize a force- and time-dependency pattern representative of their sporting background when executing a vertical SQJ. It was of interest to examine if female

TF and VO rely RGFP966 clinical trial more on a tendency of force dominance opposed to HA and BA players, as previously shown for male athletes of the same sports. A hundred and seventy-three women (20.1 ± 2.8 years, 1.71 ± 0.09 m, 65.6 ± 10.3 kg, mean ± SD for age, height,

and mass, respectively) volunteered for the study. In detail, 136 of the participants were athletes (Table 1) and were evaluated at the beginning of their competitive season, 51 were national level TF (sprinters, jumpers, and throwers), 48 were VO, 19 were HA, and 18 were BA, all competing in top leagues of their respective sport. Inclusion to the study required athletes to constantly participate in systematic training programs for a period of at least 8 years. The sample also included 37 females who were physical education students (PE) and did not participate, besides their academic courses, in a systematic training program for at least 2 years prior to the study. No previous severe lower extremity injury was reported from the participants who gave their informed consent Tryptophan synthase for participation in the study, which was accomplished according to the Institutional Research Ethics Code for the use of human subjects. Prior to the actual testing, the participants’ anthropometric data (body height, body mass, and body fat composition) were collected.31 Before testing, participants performed a 10-min cycling session at a constant pedaling velocity of 5.5 m/s with no additional load for warm-up, followed by a 10-min flexibility program. Afterward, the participants executed three bare footed maximal SQJ on a force-plate without the swing of the arms.

1). The percentages of orientation selective neurons (selectivity index > 0.33, i.e., peak:null response > 2:1) were similar in areas V1 (58/78 = 74%), PM (30/43 = 70%), and AL (31/40 = 78%). Our estimates of orientation selectivity did not depend strongly on stimulus spatial frequency (data not shown) and are not likely to depend on temporal

frequency (Moore et al., 2005). We next considered direction selectivity across areas. Strong direction selectivity (index > 0.33, i.e., peak:null response > 2:1) was evident in 69% of V1 neurons (54/78), as compared to 42% of PM neurons (18/43) and 15% of AL neurons (6/40). V1 neurons were significantly more selective for direction than PM neurons (p < 0.02, K-S selleck inhibitor test, Figures 5B and 5C and Table 2). Neurons in AL showed less direction selectivity than neurons in V1 (K-S test, p < 10−7) and in PM (p < 0.01). These differences in direction selectivity between V1, PM, and AL cannot be explained by differences in peak response strength, which did not differ across areas (Table 2, K-S tests, all p values > 0.4; see Discussion).

However, the lower direction selectivity in AL compared to PM and V1 may be explained by our use of different stimulus temporal frequencies (8 Hz in AL, 2 Hz in PM and V1; see Moore et al., 2005), which were chosen to provide comparable response efficacy in each area (Table S1). We also investigated whether responses in any of these areas were biased to specific orientations or directions. The average normalized response across all neurons showed these a significant bias (to upward and downward drifting stimuli) in area AL Carfilzomib mw (ANOVA across eight directions, p < 0.001; see Figure S5A). Similar results were observed when considering

the preferred orientations and directions of individual neurons in area AL (Figures S5B and S5C). Population directional biases were not as clear in areas PM or V1 (all p values > 0.1). Together, these data indicate strong differences in response tuning between areas AL and PM, which suggests that these areas make distinct contributions to different visual behaviors (see Discussion). We tested whether these differences in response tuning between areas were present both during trials when the mouse was stationary and trials when the mouse was moving on the linear trackball. For this analysis, we selected all neurons in which we obtained robust estimates of spatial and temporal frequency preference both while the mouse was “still” and “moving” (same criteria as in Figure 3; V1: n = 35 neurons, AL: 27, PM: 8; Experimental Procedures). Temporal frequency tuning curves for two representative neurons, during still and moving conditions, are shown in Figure 6A. Consistent with a previous study (Niell and Stryker, 2010), locomotion led to a significant increase in peak response amplitude in V1 neurons (76%; paired t test, p < 10−4; Figures 6B and 6C).