coli O157:H7, and L. monocytogenes able to grow in media supplemented with rifampicin (Rif) (Sigma-Aldrich, St. Louis, MO) at 50 μg/ml were isolated and used in experiments in which the inoculation level was near the indigenous microbiota level. Unless otherwise specified, culture media were obtained from BD (Franklin Lakes, NJ), and were supplemented with Rif. The isolates were stored at − 80 °C in tryptic soy broth (TSB) supplemented with 15% glycerol (Fisher Scientific, Fair Lawn, NJ). The single-strain inocula were prepared as described by Uesugi et al. (2006). Talazoparib research buy The frozen stock culture was streaked for isolation onto tryptic soy agar (TSA: tryptic soy broth plus 1.5% granulated agar) and

incubated at 37 ± 2 °C for 24 ± 3 h. A 10-μl sterile loop of this culture was transferred into 10 ml of TSB and incubated at 37 ± 2 °C for 24 ± 3 h; this transfer procedure into TSB was repeated once. An aliquot (1 ml) of the second overnight culture was spread over large TSA plates (150 by 15 mm) and incubated at 37 ± 2 °C for 24 ± 3 h. The resulting bacterial lawn was collected by adding 9 ml of a 0.1% peptone to each plate and scraping the surface of the plate with a sterile spreader (Lazy-L Spreader,

Andwin Scientific, Tryon, NC). The harvested cells (11 log CFU/ml) were diluted, as appropriate, with 0.1% peptone to inoculum levels ranging from 4 to 11 log CFU/ml. The five-strain mixtures of Salmonella, E. coli O157:H7, or L. monocytogenes were prepared by growing each strain separately (under the conditions described Nutlin-3 order above) and then combining equal volumes of each strain to produce the target inoculum. The populations

in the individual and final heptaminol mixed inocula were determined by serial dilution in Butterfield’s phosphate buffer (BPB) and plating onto media as described below. Inshell walnuts were inoculated as described by Uesugi et al. (2006) for almond kernels. Inshell walnuts (400 g) were weighed into a sterile bag, inoculum (25 ml) was added, and the sealed bag was shaken and rubbed by hand for 2 min. Inoculated walnuts were spread onto four layers of filter paper (57 by 46 cm sheets; Qualitative P-5 Grade, Fisher Scientific) that was placed into a lidded plastic container (leaving a 3- to 5-cm gap to allow for air exchange). Walnuts were dried under ambient conditions for 24 ± 2 h. After drying, inshell walnuts were placed in sterile plastic bags and manually mixed by shaking for 2 min. To evaluate pathogen survival on inshell walnuts, inoculated and control nuts were stored in unsealed bags within closed plastic containers held at refrigerator (4 °C) or ambient conditions for periods of 12 weeks to 3 years, depending upon the experiment. Condensate was not observed in the bags or on the walnuts during storage. Data loggers (TempTale 4, Sensitech Inc., Beverly, MA) were placed in each storage area to record temperature and relative humidity (RH).

Note that mice were free to run during playback sessions and even showed a tendency to match running to playback of visual flow—that is, in some experiments, onset of visual flow induced the animal to run. In addition, in the closed-loop configuration, visual feedback was perturbed by briefly halting visual flow for 1 s at random times Regorafenib manufacturer (Poisson distribution, with a probability of 0.25% of perturbation every 30 ms time bin, with a refractory period of 3 s). Animals

were briefly (approximately 10 s) anesthetized with isoflurane for head fixation on the ball. Animals were then allowed to get used to the head fixation and the setup and were exposed to normal visual feedback for 10–30 min. Experiments consisted of a 2 min feedback session with 1 s perturbations of visual flow at random times and a series of three to four playback sessions, each typically consisting of 2 min feedback without perturbations and 2 min

of replay of the visual flow generated by the mouse during the first 2 min feedback session (including perturbations). In initial experiments, data were not recorded during the 2 min feedback without perturbations between playback sessions. Thus, each experiment consisted of 8–16 min of recording. During all experiments, the animal’s left eye was filmed with a video camera (The Imaging Source, ATM/ATR tumor 30 fps). Pupil position and pupil diameter were extracted online with custom-programmed software based on the design of Sakatani and Isa (2007). Two-photon images were full-frame registered using a

custom-written registration algorithm. The standard deviation of brain displacement parallel to the imaging plane was 2.4 ± 0.3 μm (mean ± SEM). All data in which cells visibly moved perpendicular to the imaging plane were discarded. Cells were selected based on mean and maximum projections of the data by hand (typically the nucleus was excluded from the selection). Use of the maximum projection ensured the inclusion of all active cells, even ones that were not visible in the mean projection. This slightly biased our cell selection toward active cells. Fluorescence L-NAME HCl traces were calculated as average fluorescence of pixels lying within the cell in each frame. To remove slow signal changes in raw fluorescence traces, we subtracted the 8th percentile value of the fluorescence distribution in a ±15 s window from the raw fluorescence signal (Dombeck et al., 2007). In addition, signals were low-pass filtered at 10 Hz. ΔF/F signals were calculated by dividing raw fluorescence signal by the median calculated over the entire fluorescence distribution of each cell and then subtracting 1 from this value. To minimize the influence of movement artifacts on average fluorescence measurements, we estimated the movement-related signal noise by calculating the standard deviation σMN of the lower half of the fluorescence distribution (ΔF/F < median[ΔF/F]) for each cell individually.

Both FHA and PT were able to elicit a T cell response in vitro in a subset of the vaccinated children, by measuring the frequency of CFSEdim cells (Supplementary Figure 2C, green gate). For the proliferation of CD4+ T cells, the response to FHA was significantly higher from that of unstimulated controls, both for wP-

and aP-vaccinated children (Wilcoxon signed rank test, p < 0.05 and p < 0.01) ( Fig. 1A and B). For the CD8+ T cells, in addition to a significant proliferation in response to FHA both in wP- and aP-vaccinated children (p < 0.01), a response to PT was observed for wP-vaccinated children (p < 0.05) ( Fig. 1C and D). These results indicated selleck chemical that, although the time since the last booster vaccine was RO4929097 manufacturer significantly longer for wP- compared to aP-vaccinated children, the proliferation capacity of wP-vaccinated children in response to antigenic stimulation was at least as good as the response observed for aP-vaccinated children. Globally, the majority of the children were able to respond by CD4+ T cell proliferation to at least one of the tested Bp antigens (79%, see Section 2.4 for definition of responder), while 60% of them responded by CD8+ T cell proliferation

( Table 1). We compared Bp-specific cytokine responses of wP- and aP-vaccinated children. The nonspecific background was determined by culturing the PBMC from the same subject, for the same period in the absence of antigen, and all results are background subtracted. The frequency of CD4+ cells producing IFN-γ of in response to FHA was significantly higher for wP-compared to aP-vaccinated children (Mann–Whitney, p < 0.01), while this difference was not significant for PT ( Fig. 2A). Antigen-specific production of TNF-α was also noted for a subset of vaccinated children

but no significant differences appeared between wP- and aP-vaccinated children ( Fig. 2B). Globally, cytokine production of CD4+ T cells in response to at least 1 antigen (FHA and/or PT) was detected in 65% (IFN-γ) and 53% (TNF-α) of the children (see Section 2.4 for definition of a responder). The frequencies of cytokine producing CD8+ T cells were low as illustrated in Fig. 2C for IFN-γ, so that classification of the subjects in responders and non-responders was not possible. When the two vaccine types were compared for their capacity to induce cytokine production in response to one or both Bp-antigens, half of the aP-vaccinated children appeared to be unable to induce a cytokine response to any antigen, in contrast to only 12% for wP-vaccinated children ( Fig. 3). Due to small sample size, no statistical analysis was performed. If a child was considered responsive to an antigen when either proliferation or cytokine production was positive, 75% and 57% of the children were responsive to FHA and PT, respectively.

2% or 30.8% of hemisegments, respectively; Figure 4B). Knockdown of pbl in all muscles using 24B-GAL4 resulted in no significant ISNb pathfinding defects ( Figure 4B). To address whether pbl axon guidance and cytokinesis functions are separable, we knocked down pbl gene function using the postmitotic driver Elav-GAL4. Embryos overexpressing pbl RNAi[v35350] under the control

of Elav-GAL4 exhibited ISNb defects in 38% of hemisegments ( Figure 4B). A similar phenotype was observed with the t28343 RNAi line LBH589 under the control of two copies of Elav-GAL4. Since the GAL4/UAS system is temperature-sensitive, we allowed these embryos to develop at 29°C to increase GAL4-mediated expression of pbl RNAi and observed

an increase in the penetrance of motor axon pathfinding defects as compared to 25°C (55.8% versus 41.2%; Figures 4B, S3C, and S3D). These data strongly suggest that neuronal Pbl is required postmitotically for normal motor axon pathfinding. Since we observed that p190, like Pbl, also exhibits a strong physical association with Sema-1a and that two potential p190 enhancer GAL4 lines drive reporter expression in the CNS ( Figures S3H–S3J), we examined the role played by p190 in motor axon pathfinding using transgenic RNAi lines ( Billuart et al., 2001). Overexpression of the p190 RNAi transgene using Elav-GAL4 resulted in premature defasciculation of ISNb axons prior to reaching muscle

13, and sometimes muscle 6: reflecting either increased defasciculation or a defect in muscle target recognition (∼20% selleck kinase inhibitor of hemisegments; Figures 3J, 3K, 4C, and S6). This premature branching phenotype was rescued to wild-type levels when one copy of a UAS-mycp190 transgene ( Billuart et al., 2001) was introduced along with p190 RNAi Ribonucleotide reductase (5.9% of hemisegments; Figure 4C). Furthermore, when premature branching is observed in wild-type embryos it is qualitatively distinct from what we observe following p190 LOF, often occurring between the ventral and dorsal surfaces of muscle 13 rather than prior to ISNb arrival at muscle 13 (compare arrowhead in Figure 3A to arrows in Figures 3J and 3K). In addition, premature ISNb branching phenotypes qualitatively and quantitatively similar to those we observe in p190 RNAi lines were noted in p1902 maternally and zygotically-derived null alleles, and total ISNb defects were significantly rescued by reintroduction of the neuronal mycp190 transgene ( Figure 4D). These results show that neuronal p190 is required postmitotically for motor axon pathfinding. To test whether pbl plays a role in Sema-1a-mediated motor axon guidance, we investigated genetic interactions between pbl and Sema-1a, PlexA, and PlexB. When either a PlexA or PlexB null allele was introduced into pbl2 heterozygotes, total ISNb and premature branching defects were not significantly affected.

g. O. jakutensis ( Plenge-Bönig et al., 1995)] or worm nest [e.g. W. bancrofti ( Norões et al., 1997)], apparently preventing the accumulation of leukocytes on the worms’ surface. In these species, there is no evidence that Wolbachia is involved in immune evasion, and its role may ‘simply’ be metabolic provisioning, although clearly there are filarial

taxa that thrive without it. Secondly, the Onchocerca spp. with degenerated musculature in the female and a sessile lifestyle in fibrous nodules (O. ochengi, O. volvulus and Onchocerca gibsoni) may depend on a Wolbachia-mediated “immunological blockade”, comprising a local neutrophilia that interferes with eosinophil infiltration and degranulation ( Nfon Selleck BVD523 et al., 2006). The only known Wolbachia-negative Onchocerca spp., O. flexuosa, may utilise a third strategy as the females are sessile in fibrous nodules, yet do not invoke a neutrophilic response ( Brattig Selleckchem NLG919 et al., 2001). Evidence from partial genome sequencing has demonstrated that this species once harboured Wolbachia ( McNulty et al., 2010). One mechanism by which

it may have compensated for loss of the endosymbiont is to have accelerated its development to sexual maturity, as it appears to have a much shorter lifespan than the Wolbachia-positive nodular species ( Plenge-Bönig et al., 1995). Females of Onchocerca spp. that do not form nodules and which have retained a well-developed somatic musculature

[e.g. O. gutturosa ( Franz et al., 1987)] are probably not as active as L. loa, but nevertheless, may retain the ability to dislodge host effector cells by sloughing and thus express a variation of the first strategy. Chodnik (1957) suggested that O. armillata is a motile species due to the many vacant tunnels within histological sections. This is in accordance with the histological observations and the experience of manual extraction of adult worms from the aorta wall in our study. Furthermore, the musculature of adult O. armillata female worms is prominent Oxalosuccinic acid ( Franz et al., 1987), and the immunological reaction described in the current study (i.e., dominated by macrophages and giant cells, with small numbers of granulocytes more distant) is similar to that reported for O. gutturosa, although it may be less intense ( Wildenburg et al., 1997). The vascular injury noted here and also by Chodnik (1957) provides further support for a nomadic lifestyle for O. armillata. However, definite evidence to support this hypothesis has not been obtained, as it would be extremely difficult to visualise adult worms in vivo in the deep anatomical location of the aorta. The high prevalence (90.7%) of O.

Expression of UAS-mys-RNAi or UAS-mew-RNAi in the wing causes severe wing blister (data not shown), a hallmark of defective integrin signaling ( Brower, 2003). We knocked-down mys and mew in da neurons with Gal421-7 ( Song et al., 2007) and examined the spatial relationship Selumetinib of class IV da dendrites and the ECM in third instar larvae. The ddaC dendrites at the dorsal midline are usually attached to the ECM, with only 1.75% of dendritic length enclosed in the epidermis ( Figure 3J). In RNAi control neurons with only UAS-Dicer-2 (UAS-Dcr-2)

expression ( Dietzl et al., 2007), the enclosed dendritic length is increased to 5.69% ( Figure 3F). In contrast, with mys or mew knockdown, the enclosed dendritic length is MDV3100 cost increased to 24.33% or 28.32%, respectively ( Figures 3G, 3H, 3I, and Movie S2), suggesting that defective positioning of dendrites is the underlying cause of the increased noncontacting dendritic crossings. Integrins function by forming heterodimers of α and β subunits. If integrin α subunit Mew and β subunit Mys regulate dendrite positioning by forming a functional dimer, mutant alleles of mew and mys may genetically interact with each other. Indeed, in transheterozygotes of mys1 and mewM6, the percentage of enclosed dendrites is increased to 22.62%, compared to 4.09% in mys1/+ and 4.18% in mewM6/+ ( Figures 3K–3N). Collectively, these data show that integrin genes mew and mys are important for attaching the class IV da

dendrites to the ECM and thus for nonoverlapping coverage of dendritic fields. Since removal of mys and mew from class IV da neurons causes detachment of dendrites from the ECM, we tested if supplying more integrins in the dendrites promotes attachment to the ECM, by expressing UAS-mys and UAS-mew, individually or in combination, in class IV da neurons. Overexpression of Mys, but not Mew, in class IV da neurons causes significant dendritic reduction ( Figures S1A and S1B). Expressing Mys and Mew simultaneously largely rescues the dendritic reduction associated with Mys overexpression ( Figure S1C). Because Mys and Mew function as heterodimers and the balance of their dosages is likely important, we

further analyzed the animals in which both Mys and Mew are overexpressed in class IV da neurons. At the ventral Suplatast tosilate midline, the percentage of enclosed dendrites of vdaB is 8.43% ( Figures 4A and 4C) in the wild-type control. In contrast, Mys and Mew coexpression in vdaB completely eliminated the dendrite enclosure and associated noncontacting dendritic crossing ( Figures 4B and 4C), suggesting that Mys and Mew mediate the attachment of dendrites to the ECM. Since studies of loss or gain of integrin function implicate Mys and Mew activity in dendrites, including terminal branches, we asked whether Mys and Mew are localized on class IV da dendrites. Unfortunately, the high levels of epidermal expression of Mys and Mew at the basal surface (Figures S1D–S1E″) render it difficult to distinguish Mys and Mew on dendrites.

Z scores greater than 1.96 or −1.96 indicated significant changes in coherence for the color and orientation rule, respectively (see Supplemental Information for details). Time-frequency regions of interest (e.g., the “alpha” and “beta” bands) were defined such that they encapsulated the peaks in rule-selective changes in synchrony ( Figures 2 and S3). Although the bands were not predefined, they closely follow the alpha and beta bands

defined in other studies, supporting conclusions about common mechanisms (see Discussion). Phase-locking value (PLV) Roxadustat was used to estimate spike-field synchrony. The phase locking of task-relevant neurons (as identified by ωPEV, see above) to the LFP of electrodes participating in either the color or orientation network was estimated in a 200 ms window around the time of stimulus onset (−50 ms to 150 ms). In order to correct for the strong sample size bias in estimating spike-field synchrony, a stratification procedure was used (requiring

200 spikes in the window). Significant differences were determined by a permutation test, as above (see Supplemental Information for details). The relationship between rule-dependent LFP synchrony and reaction time was determined by first regressing out the effect of preparation time on reaction time (see Supplemental Information Selleck CAL 101 for details). The resulting reaction time residuals were sorted into “fast” and “slow” trials (defined as the 65th–95th and 5th–35th percentile of the residual distribution for each session, respectively). As

above, a permutation test was used to estimate a Z score of the observed rule-selective differences in synchrony (see Supplemental Information for details). Significant differences in rule selectivity between fast and slow trials were determined by comparing the average absolute Z score in the beta (or alpha)-frequency bands using a Wilcoxon signed-rank test. To preclude dependence between electrodes recorded in the same session, we bootstrap resampled the electrode pairs 1,000 times. After establishing that rule selectivity was stronger on average in the alpha and beta bands, respectively, we examined rule selectivity for differences over time by testing for differences in rule selectivity at each time point, again using a Wilcoxon signed-rank test (see Supplemental Information Phosphoprotein phosphatase for further details). This work was supported by NSF CELEST grant GC-208001NGA and National Institute of Mental Health grant P50-MH058880. We thank S. Henrickson, S.W. Michalka, and M. Wicherski for comments on the manuscript and W. Asaad, J. Roy, and M. Siegel for technical support. E.K.M. conceived of and designed the experiment; C.D. designed the experiment, trained monkeys, and collected neural data; and T.J.B. and E.L.D. conceived of, implemented, and executed data analysis; T.J.B., E.L.D., D.B., and E.K.M. wrote the manuscript.

7 Unlike Kalenjin adults that grew up barefoot, habitually barefoot Kalenjin adolescents, and habitually barefoot U.S. adults, Hadza runners never used FFS in trials recorded for this study. Due to the mix of MFS and RFS among the Hadza, mean plantar foot strike angle among adults was intermediate between selleck chemicals llc habitually

shod U.S. adults and Kalenjins. U.S. adults ran with a high frequency of RFS, thus leading to the large dorsiflexion upon plantar foot strike, causing smaller (negative) foot angles. Kalenjins had a high frequency of FFS, thus showing the large plantarflexion upon foot strike and larger angles. Ankle angles among Hadza adults were similar to those of habitually barefoot U.S. adults, barefoot Kalenjin adolescents, and Kalenjin adults who grew up

barefoot. Knee angles at foot strike were consistently greater (i.e., more flexed) among Hadza adults than for Kalenjin or U.S. groups. The difference in knee Selleckchem MK2206 angle is more substantial when differences in running speed are considered; Hadza speeds were lower, on average, than those of the Kalenjin or U.S. groups reported by Lieberman and colleagues,6 yet knee flexion generally increased with speed in our sample. Direct comparison of joint angles among studies is hampered by the different methods used to measure them. Unlike Lieberman and colleagues,6 we did not place visual markers on anatomical landmarks. Instead, the knee angle in our study was calculated using the major axes of the thigh and shank, which may have resulted in systematic differences in knee angle calculation relative to the analysis of Lieberman and colleagues. The image resolution and lack of visual markers probably also decreased the precision of our angle measurements, an effect that was most evident in our inability MRIP to distinguish plantar angles ±1° for MFS trials (Fig. 2). Thus, while we took care to calculate angles in a manner that would maximize comparability to other studies (Fig. 1), it is possible that some differences between

studies arise from methodological differences. Foot strike behavior among traditional Hadza hunter-gatherers was mixed, with consistent differences between men and women and between juveniles and adults. Women and juveniles used RFS more often than MFS, while men used MFS almost exclusively. There was no difference between shod versus barefoot conditions, nor among respirometry trials (which lasted for several minutes) and short-bout trials (which lasted a few seconds). The lack of difference between short-bout and respirometry trials lends confidence that the duration of the trial did not affect foot strike choice. Further, there is no evidence that Hadza adults switched from RFS to MFS as speed increased. While the Hadza used MFS rather than FFS, comparisons with other populations suggest that Hadza men are similar to experienced barefoot runners such as the Kalenjin in avoiding RFS.

PFC interneurons, hippocampal cells, and putative VTA GABAergic cells did not show such task-dependent phase locking. The fraction of significantly buy PFT�� theta phase-locked neurons in each brain region was similar in the two tasks (Figure 5). These findings show that the magnitude of 4 Hz modulation of PFC pyramidal cells and VTA dopaminergic cells was task specific. Although changes in 4 Hz and gamma oscillations in both PFC and VTA were reliably correlated with the working-memory component of the task, they did not predict the directional choice of the animal on a given trial (p > 0.05 for

each rat). In contrast, a sizeable fraction of both PFC and hippocampal cells fired at significantly different rates in the central arm on trials with future left and right turns (Figure 6A). Because such goal-predicting, “prospective,”

or “episode” neurons have been suggested to be a part of the working-memory network (Wood et al., 2000, Frank et al., 2000, Fujisawa et al., 2008 and Pastalkova et al., 2008), we examined their relationship with LFP oscillations and compared them with nonpredicting but active neurons in the 0.0–0.3 segment of the central arm, in which movement trajectories and speed during left and right trials were indistinguishable (Fujisawa et al., 2008). For these comparisons, only neurons that fired at least 1 Hz in the central arm were included. The fraction of both 4 Hz and theta-modulated neurons was significantly higher in the goal-predicting PFC pyramidal cell group (Fujisawa Galunisertib mouse et al., 2008), as compared to nonpredicting cells (Figure 6B). Furthermore, below the magnitude of phase locking of the goal-predicting PFC pyramidal cells to 4 Hz and theta oscillations was also significantly higher than phase locking of the nonpredicting neurons (Figure 6C). This difference could not be explained by the significantly lower firing rate of nonpredicting neurons

in the central arm because the phase-modulation differences persisted after equalizing the spike numbers of all predicting and nonpredicting neurons for the analysis, using exhaustive bootstrapping (Vinck et al., 2010; Figure S6). Although the fraction of predicting neurons in the hippocampus and PFC was similar, hippocampal predicting and nonpredicting neurons did not show differential phase locking to 4 Hz or theta oscillations (Figure S6). Because timing of neuronal spikes was biased by both 4 Hz and theta rhythms, we also examined their joint effects. First, we tested whether there is a phase relationship between these oscillations. The PFC 4 Hz trough (180°) was significantly locked to the trough (198.5° ± 3.78°) of CA1 theta waves in each rat (Figure 7A; p < 0.01; shift predictor statistics).

ANOVA was used to examine variation across multiple groups with post hoc Dunn’s multiple comparison tests. Two-tailed Spearman’s test was used to compare correlations. One-sample and paired t tests were used for comparisons of clustering, distribution, and docking. To compare the total spatial distribution of PC+ versus PC− vesicles (Figure 4H), we computed the difference between the spatial frequency histograms. This was done on a bin-by-bin basis for the bins with the highest 70% frequencies of the PC+ cluster (i.e., the spatial area encompassing 70% of PC+ vesicles). The distribution of differences was then tested with a one-sample t test under the null

hypothesis that the mean difference was 0. The alpha value of 0.05 was used for all statistical comparisons. To investigate the effect of preferential reuse of recycling vesicles INCB018424 in vitro on FM dye destaining curves, we implemented a stochastic model of vesicle release in Python. The model had a recycling pool of 40 vesicles, with a release probability of 0.15 and a recycling time of 10 s. All recycling vesicles were initially labeled

as FM positive, and the synapse was stimulated at 10 Hz GSK126 chemical structure while monitoring the decrease in the number of FM-positive vesicles. The fraction of reuse was varied between 100% and 0% by drawing vesicles from a pool with the desired fraction of FM-positive and FM-negative vesicles. Statistical comparison between the model and experimental data used a two-sample t test for each time point, and mean alpha value for the whole curve was then calculated. The mean alpha value was >0.05 for reuse fractions between 95% and 80%, and the highest value was for 88% reuse (p = 0.28). This work was supported by Wellcome Trust (WT084357MF) and BBSRC (BB/F018371) Phosphoprotein phosphatase grants to K.S and by grants from the Gatsby Charitable Foundation, the ERC, and the Wellcome Trust to M.H. “
“It has long been

reported that nearby cells in many cortical areas exhibit correlated trial-to-trial response variability (referred to as “noise” correlations), possibly originating from common synaptic input (Bair et al., 2001; Kohn and Smith, 2005; Shadlen and Newsome, 1998). Estimation of correlated neuronal firing is fundamental for understanding how populations of neurons encode sensory inputs. Indeed, the structure of correlations across a network has been shown to influence the available information in the responses of a population of cells (Abbott and Dayan, 1999; Sompolinsky et al., 2001; Cafaro and Rieke, 2010) and possibly limit behavioral performance (Abbott and Dayan, 1999; Cohen and Newsome, 2008). In addition, correlations between neurons can serve to constrain the possible schemes employed by the cortex to code and decode sensory stimuli depending on the stimulus or behavioral context (Ahissar et al.