As predicted by the cbDDM, for trials in which subjects took more time to make a decision, the response in OFC generally increased with a shallower slope and commenced later in the trial. There was both a main effect of time (p =

0.024) and a condition-by-time interaction (p = 0.027), demonstrating faster rates of increase for shorter trials. Similar OFC time series profiles were observed when the analysis was restricted either to mixtures of the same difficulty level (Figure S4) or to correct trials only (Figure S5), supporting the rationale behind combining trials of different stimulus difficulty and further confirming DDM predictions. The current results suggest that humans integrate olfactory perceptual evidence in order to enhance perceptual decision-making. These findings were supported across two independent psychophysical experiments. First, in a fixed-sniff paradigm, choice accuracy improved A 1210477 when subjects were given an opportunity to make more sniffs, especially

for difficult odor mixtures (Figure 1C). This behavioral profile accords with temporal integration. Second, in an open-sniff paradigm, a drift-diffusion model of integration accounted for the resulting RT distributions significantly better than did a nonintegrative (stochastic) model (Figure 3D). This effect was particularly HDAC inhibitor true when the simulation model incorporated decision bounds that collapsed over time (Figure 4). The use of two complementary paradigms was necessary to establish that information accumulates in the human olfactory system. In the open-sniff paradigm, subjects only make a choice once a decision bound is reached, effectively clamping performance accuracy. This has the benefit of generating RT distributions that can be compared to model-derived RT distributions, such as the DDM, to provide evidence for or against integration. However, the open-sniff task is unable to demonstrate the type of choice-accuracy profiles that would be in keeping with integration. On the other hand, in the fixed-sniff

paradigm, subjects make a response at a specified time, effectively disengaging their choices from a decision criterion. This has the potential benefit of eliciting behavioral accuracy profiles reflective of integration over time, although the resulting RT distributions (arising from imposed trial Phosphatidylinositol diacylglycerol-lyase lengths) cannot be used to model integrative processing mechanisms. Together these two paradigms provide converging evidence that the human olfactory system, like other sensory systems, can integrate perceptual information. Brain imaging data highlighted a corresponding fMRI signature of temporal integration in the OFC. Using a regionally unbiased approach, we found that odor-evoked activity in both right and left medial OFC conformed closely to integration profiles as predicted from the DDM (Figure 5). Specifically, time series increased at slower rates for longer trials, peaked at the time of decision, and had lower peaks for longer trials.

The extent of endogenous NLG1 loss from synapses observed using biochemical methods is greater than that observed by immunostaining (Figure 1). This disparity may be attributed to the broad specificity of the pan-NLG antibody used for immunolabeling and to the fact that it targets the C-terminal domain of NLGs, an epitope that is further regulated by the γ-secretase complex (Figures S3E and S3F). It will be important

to TSA HDAC address how other NLG isoforms are regulated by MMPs and whether NLG1-CTFs participate in intracellular signaling. Multiple soluble NLG1-NTF species can be detected in the brain (Figure 2D), suggesting that NLG1 contains more than one cleavage site. This observation provides a plausible explanation for why single amino acid point mutations in the juxtamembrane region of NLG1 fail to prevent MMP-dependent cleavage, which instead

requires substitution of a 24 amino acid segment (Figures 4A and 4B). Moreover, basal levels of NLG1-NTFs can be detected in brain extracts from MMP9 KO mice (Figure 7B), indicating the existence of MMP9-independent mechanisms cleaving NLG1. In addition, our data indicate that NLG1-NTFs are most abundant during the first postnatal weeks (Figures 2G and 2H), suggesting that NLG1 cleavage see more may have different functions during development. It will be important to define in detail the activity-independent and MMP9-independent mechanisms of NLG1 cleavage and their specific role in synapse development and plasticity. Nevertheless, our results indicate that MMP9 is required

for activity-dependent cleavage of NLG1 in multiple cellular contexts in vivo (Figure 7) and in vitro (Figures 3 and 4), consistent with the known involvement of MMP9 in multiple forms of synaptic plasticity (Bozdagi et al., 2007; Nagy et al., 2006; Szklarczyk et al., 2002; Wang et al., 2008; Wilczynski et al., 2008). Focal uncaging of glutamate triggers MMP9-dependent cleavage of postsynaptic NLG1, indicating Adenosine that this mechanism is regulated locally (Figures 4C and 4J). Interestingly, we detected a small heterosynaptic decrease of GFP-NLG1 from neighboring dendritic spines after synaptic stimulation (Figures 4C and 4J), suggesting that MMP9 activation may spread to adjacent dendritic regions. It remains unclear how NMDAR/CaMK signaling couples to MMP9 activity; however, considering the presence of MMP9 in spino-dendritic tubulovesicular structures (Wilczynski et al., 2008), one possibility is that CaMK activation triggers exocytosis of MMP9-containing vesicles in nearby dendritic regions or spines (Kennedy and Ehlers, 2011). It will be interesting to address if persistent cleavage of NLG1 can induce dendrite-wide effects and how the surface pools of NLGs are redistributed and replenished following periods of increased MMP-9 activity.

, 2010). Such signals can be combined within the area’s circuitry

with incoming sensory information into a saliency map that reflects the organism’s priorities and goals. Signals originating within this map can then modulate (via direct or indirect pathways; Petrides and Pandya [2007]) the responses of neurons in sensory areas representing target and distracter features (Ardid et al., 2007, Gregoriou et al., 2009, Olivers, 2008 and Rainer et al., 1998). One question that remains to be answered is whether there is a distinctive role for dlPFC and FEF neurons in attentional control. One possibility is that the dlPFC plays a role in forms of attentional modulation that require selectivity for nonspatial features of visual stimuli

(i.e., feature-based-attention; Bichot et al., 2005 and Treue and Martinez Trujillo, click here 1999; or object-based attention; Roelfsema et al. [1998]), whereas the FEF plays a role in selleck compound allocating spatial attention (Moore and Armstrong, 2003). Favoring this hypothesis, selectivity for nonspatial features such as motion direction has been documented in dlPFC neurons (Zaksas and Pasternak, 2006). A second possibility is that the dlPFC integrates signals from different sensory modalities into a single saliency map and then signals FEF neurons the target and distracter locations. Favoring this idea, it has been recently reported that neurons in the ferret prefrontal cortex shape the flow of auditory information during a behavioral task (Fritz et al., 2010). In sum, our results agree with previous studies reporting that dlPFC neurons encode the allocation of attention through their

firing patterns (Boussaoud and Wise, 1993, di Pellegrino and Wise, 1993, Everling et al., 2002, Lebedev et al., 2004 and Rainer et al., 1998). Importantly, they further support a role of the primate prefrontal cortex on inhibitory control of behavior (Aron et al., 2004, Hasegawa et al., 2004 and Sakagami et al., 2006). We found that the response suppression of distracter representations in these units produces changes in their filtering performance similar to the ones observed in the organism’s behavior. It remains to be determined what the exact neuron-to-neuron interactions within dlPFC networks underlying the observed patterns of response suppression, are as well why as whether manipulating such interactions leads to changes in behavioral performance. Two young adult male monkeys (Macaca mulatta, Ra: 7 kg; Se: 9 kg) participated in the experiments. During the training and testing periods, the animals received their daily amounts of fluids (fruit juice) as reward for correctly performing the task. The average fluid intake during a session was between 300 and 400 ml. We also gave the animals fresh fruits as supplement when finishing a session. Body weights were measured on a daily basis to monitor health and growth.

coli O157:H7, S. Typhimurium, and L. monocytogenes. Patil et al. ON-01910 chemical structure (2010b) studied the antimicrobial efficacy of gaseous ozone against E. coli in apple juice of various pH levels. However, there have

been very few research studies investigating the bactericidal effect when apple juice is treated with both heat and ozone gas simultaneously and their effect on quality changes of apple juice. Therefore, in this study, we investigated the combination or synergistic effect of ozone and heat treatments on apple juice to inactivate E. coli O157:H7, S. Typhimurium, and L. monocytogenes. Also, changes in color and residual ozone of apple juice after treatment were investigated. Strains of E. coli O157:H7 (ATCC 35150, ATCC 43889, ATCC 43890), S. Typhimurium (ATCC 19585, ATCC 43971, DT 104), and L. monocytogenes (ATCC 19114, ATCC 19115, ATCC 15313) were obtained from the bacteria culture collection of Seoul National University (Seoul, Korea). Stock cultures were prepared by combining 0.7 ml of Tryptic Soy Broth (TSB; Difco, Becton Dickinson, Sparks, MD, USA) and 0.3 ml of 50% glycerol

and storing at − 80 °C. Working cultures were streaked onto Tryptic Soy Agar (TSA; Difco), incubated at 37 °C for 24 h, and stored at 4 °C. Each strain of E. coli O157:H7, S. Typhimurium, and L. monocytogenes was cultured in 5 ml TSB at 37 °C for 24 h, harvested by centrifugation at 4000 g for 20 min at 4 °C and washed three INCB024360 in vivo times with sterile 0.2% peptone (Bacto, Sparks, MD). The final pellets were resuspended in 0.2% sterile peptone water, corresponding to approximately 108–109 CFU/ml. Mixed culture cocktails were prepared

by blending together equal volumes of each test strain. Pasteurized apple juice was purchased at a local supermarket (Seoul, Korea) and stored at 4 °C. One hundred milliliters of apple juice was dispensed into a 500 ml bottle and 0.1 ml of antifoam B emulsion (Sigma Aldrich, Ireland Ltd.) was added to the apple juice to prevent excess foaming. Apple juice was inoculated with 0.1 ml of the mixed culture cocktail (E. Resminostat coli O157:H7, S. Typhimurium, and L. monocytogenes). The final cell concentration was 105–106 CFU/ml. As shown in Fig. 1, ozone gas was produced by an ozone generator (Ozonetech Co., Ltd, Korea) at generation rates of 2.0–3.0 g/m3 from ambient air at a flow rate of 3.0 l/min. The concentration of ozone was controlled by an ozone monitor (Okitrotec Co., Japan). Ozone was pumped directly into the juice through a delivery tube and sparged through a perforated tube into a 500 ml bottle. As soon as the preset temperature (25, 45, 50 and 55 °C) was stabilized by using a water bath, heat treatments were conducted. Juice samples not subjected to ozone treatment, but heat treated, were designated as the heat treatment alone group. Each apple juice sample treated at 25 °C without or with ozone was regarded as control group for confirming the effect of heat and ozone at 25 °C.

Nevertheless, to rule out this possibility, we examined the time course of the baseline modulations time-locked to cue offset. These time courses were indistinguishable between the three attentional states (Figure S4), demonstrating that the attentional modulations (which are time-locked to stimulus onset) are not due to direct visual responses

to the cue. Second, systematic differences in fixational eye movements between the attentional states could have contributed to the observed variations in V1 responses. This possibility seems unlikely given that the attentional IGF-1R inhibitor modulations start before the stimulus-evoked responses (Figure 6). Nevertheless, to rule out this possibility, we compared several eye position statistics in the three attentional states. Our results reveal no significant differences in these statistics depending on the attentional condition (Figure S5), providing further support for the top-down nature of the observed modulations. What is the purpose of the observed attentional modulations? One possible goal of attention is to allocate limited representational resources based on task demands (e.g., Broadbent, 1958). Another possible

goal of attention is to limit the access of task-irrelevant stimuli to circuits that control behavior (e.g., Allport, 1993). If the representation of multiple visual targets in V1 was a limited resource that could be controlled by attention, we would have expected V1 target sensitivity at attended locations to be higher under focal attention than under www.selleckchem.com/products/DAPT-GSI-IX.html distributed attention (Figures 1C and 1D). Our finding that V1 population responses at attended locations are indistinguishable under focal and distributed attention suggests that in our task, and at the level of neural populations, target sensitivity in V1 may not be a limited resource that can be enhanced by focal attention. We find that behavioral performance is improved under focal attention relative Isotretinoin to distributed attention (Figures 2B–2D). As illustrated by our toy example (Figure 1), behavioral improvement

under focal attention is expected even if V1 target sensitivity is not limited and is identical in focal and distributed attention. A simple analysis based on signal detection theory shows that the observed behavioral improvement in accuracy under focal attention is consistent with no changes in neural sensitivity under focal and distributed attention (Suppl. Figure 6; see also Eckstein et al., 2000, Palmer et al., 2000 and Pestilli et al., 2011). This analysis, therefore, provides further support to the hypothesis that in our task, target sensitivity is not a limited resource that can be enhanced by focal attention. While our physiological and behavioral results appear to be inconsistent with attention as a mechanism for allocating limited resources in V1, we cannot rule out the possibility that such a mechanism operates in V1 in other tasks.

Thus, topographic information for axon-target interactions within the MNTB are preserved, even when axons form

synapses in the wrong hemisphere. However, functional maturation of the synaptic contacts was severely impaired. In wild-type animals, calyx of Held synapses acquire characteristic morphological and functional properties during the first 3 postnatal weeks. Each MNTB neuron is DAPT price innervated by a single calyx, and calyces exhibit extraordinarily fast transmitter release properties. In Robo3 conditional knockout mice, the ipsilaterally misplaced synapses were markedly underdeveloped by functional and morphological criteria. In 9- to 12-day-old animals, MNTB neurons were innervated by multiple smaller calyx-like terminals. Evoked transmission was severely reduced, and synapses showed immature forms of synaptic plasticity. In adolescent and adult animals, some of these defects were corrected, as multi-innervation receded and synapse size appeared normal. However, synaptic transmission remained strongly reduced, most likely due to a persistent decrease in the fast-releasable

pool of synaptic vesicles. A key question resulting from these findings is whether synapse development is indeed altered due to a failure of commissural neuron reprogramming after midline crossing or whether Robo3 has a postnatal selleck chemicals function in synaptogenesis. Robo3 is strongly downregulated during late embryonic development and not detectable during the postnatal period when calyces develop (Michalski et al., 2013). Moreover, conditional ablation of Robo3 at the time

of birth did not alter synaptogenesis. Thus, the postnatal defects in synapse maturation are indeed a consequence of the Robo3 loss-of-function during embryonic development. The authors propose that axon midline crossing “conditions” synapse maturation. According to this model, midline crossing Isotretinoin would be a prerequisite for normal synapse development due to reprogramming of gene expression and/or protein trafficking in the commissural neurons. An additional interpretation would be that the inappropriate ipsilateral convergence of VCN-derived information with other neuronal activities causes the developmental changes. However, phenotypes emerge before hearing onset (postnatal day 12), and other synapses such as MNTB-LSO connections develop normally. This supports a rather selective defect in the misrouted VCN-MNTB connections. The key targets of the presumptive midline-dependent re-programming remain to be identified. However, several molecular signals that direct the growth and functional properties of calyx of Held synapses have emerged in recent studies. Thus, mouse mutants lacking the active zone proteins RIM1 and RIM2 exhibit a reduction in the fast-releasable pool of synaptic vesicles (Han et al., 2011).

Prepro-VIP level was increased significantly in the brain of Eif4ebp1 KO mice (normalized band intensities: KO versus WT, 3.88 ± 0.36 versus 1 ± 0.18, p < 0.05, Student’s t test;

Figure 5C). In contrast, expression of VPAC2 (the VIP receptor expressed in the SCN), and of the precursor proteins of other neuropeptides implicated in the SCN synchrony ( Piggins et al., 1995 and Maywood et al., 2011), including prepro-GRP and prepro-AVP, was not changed ( Figure 5C). In addition to the neuropeptides, we examined other proteins involved in SCN synchrony, including GABAa receptor ( Liu and Reppert, 2000, see more Colwell et al., 2003 and Albus et al., 2005) and gap junction protein Connexin 36 ( Long et al., 2005). The levels of Connexin 36 and the GABAa receptor α subunit were not altered in the Eif4ebp1 KO brain ( Figure 5C). Furthermore, the expression of the 4E-BP1 binding partner, eIF4E, was not changed ( Figure 5C). These results demonstrate specific regulation of prepro-VIP by 4E-BP1. To complement the in vivo data, we studied prepro-VIP expression in mouse Neuro2A and human SHEP neuroblastoma cells (Waschek et al., 1988). Treatment of Neuro2A cells with the specific mTOR active-site inhibitor, PP242, resulted in reduced prepro-VIP levels and in dephosphorylation of 4E-BP1 Ion Channel Ligand Library after 3 hr (Figure S4B). To determine whether the effect of mTOR inhibition on prepro-VIP expression is dependent on 4E-BP1, we knocked down

4E-BP1 in SHEP cells using lentivirus (Figure S4C). Prepro-VIP was increased by ∼1-fold in 4E-BP1 knockdown cells. Rapamycin decreased 4E-BP1 phosphorylation and inhibited prepro-VIP

expression in control cells (scrambled), but not in 4E-BP1 knockdown cells (sh4e-bp1) (Figure S4C). Serum stimulation induced strong prepro-VIP expression in control cells, but to a lesser extent in 4E-BP1 knockdown cells (Figure S4D), indicating that inducible prepro-VIP expression is at least partially dependent on 4E-BP1. Consistent with these data, overexpression of 4E-BP1 led to a reduction in prepro-VIP (Figure S4E). Overexpression of WT eIF4E, but not the W56A mutant, which cannot bind to the mRNA cap (Gingras et al., 1999), increased prepro-VIP (Figure S4F), demonstrating that prepro-VIP synthesis is dependent on eIF4E and cap-dependent translation in neuroblastoma cells. Expression of Vip 5′ UTR-RLuc mRNA, but not RLuc or Grp 5′ Phosphoprotein phosphatase UTR-RLuc mRNA, was enhanced in Eif4ebp1 KO (∼2-fold) as compared to WT mouse embryonic fibroblasts ( Figure S4G; p < 0.05, ANOVA). Grp mRNA 5′ UTR has a similar length but lesser secondary structure than Vip mRNA 5′ UTR. Thus, these results demonstrate that Vip mRNA translation is preferentially enhanced in 4E-BP1 KO cells. Because 4E-BP1 inhibits translation initiation, it was anticipated that prepro-VIP upregulation in the Eif4ebp1 KO brain is at the mRNA translation initiation step. To demonstrate this, we studied Vip mRNA translation by polysome profiling.

This dependence on NMDA receptor activation for induction of locomotor-like activity suggests that the burst-like properties that NMDA receptor activation can evoke in spinal neurons (Hochman et al., 1994 and Ziskind-Conhaim et al., 2008) is a requirement

for rhythm generation in the Vglut2-KO mice. The rhythm generation, therefore, seems to be a consequence of the interplay between cellular rhythmogenic properties and reciprocal inhibitory coupling between groups of inhibitory neurons, similar to what has been observed in many invertebrate motor networks (Marder and Calabrese, 1996) and in the mammalian cortex (Bartos et al., 2007). The fact that slow low-amplitude oscillations were seen in individual root recordings after blocking inhibition suggests that even MNs may display NMDA-induced oscillations, similarly to what was previously FK228 purchase described Z-VAD-FMK mw (Tresch and Kiehn, 2000). Notably, the frequency of the rhythm in Vglut2-KO mice was restricted to the lower part of the frequency spectrum (<0.4 Hz) reported for locomotor-like activity in the neonatal mouse (Talpalar and Kiehn, 2010), and for any given drug concentrations the frequency always remained lower in the Vglut2-KO compared to the control littermates. These observations suggest that, although the rIa-IN networks can generate a rhythm, this is not the normal state in

an intact locomotor network. Rather, the rIa-INs may be driven into rhythmicity by upstream flexor- and extensor-related excitatory CPG neurons (Kiehn, 2011 and McCrea and Rybak, 2008). These rhythmogenic excitatory networks may be connected via inhibitory neurons that are different from the rIa-INs (see Kiehn, 2011). We anticipate that under normal circumstances these excitatory circuits produce and pace the rhythm. However, when the Vglut2-dependent neurotransmission is removed, the rhythm generation can be shifted to the Ia inhibitory networks.

These latter networks could only be brought to bursting when stimulated with drugs and could not be accessed by the neural locomotor initiating signals. In this sense, the rhythmogenic capability of Ia inhibitory networks in the Vglut2-KO mice is a consequence of the removal of the excitatory network components. Our experiments, therefore, stress these the need for a careful and intervening analysis in order to understand the significance of changes in network structure when mouse mutants are investigated in the in vitro conditions and when locomotor-like activity is induced by drugs. The details of generating the Vglut2 knockout mice are reported elsewhere (Supplemental Experimental Procedures; Hnasko et al., 2010). The generation and specificity of the BAC-Vglut2-Chr2-YFP mouse is described in Hägglund et al. (2010). ROSA26-Cre-ER™ mice were obtained from Jackson Laboratory. The procedure for inducing Cre is described in the Supplemental Experimental Procedures.

, 2007). Thus, albeit encouraging, our positive results with C. schoenanthus have to be interpreted with caution and tested in vivo to confirm or refute our in vitro results, and within the realm of host–parasite interactive physiology, biochemistry, compound availability or toxicity. “
“Toxoplama gondii has been described as one of the most significant causes of reproductive disorders in flocks of sheep around the world ( Dubey, 1986). Miscarriages are the main kind of reproductive failure, generating considerable economic losses ( Silva and Silva, 1988 and Buxton et al., 2007). Laboratory diagnosis of the infection is of fundamental importance because

reproductive failure can result from a variety of other infectious diseases ( Vidotto, selleck screening library AZD8055 datasheet 1992 and Amato Neto et al., 1995). In pregnant sheep, during acute infection, the placenta is invaded by tachyzoites, in the free form and inside trophoblasts,

resulting in necrosis and mineralization of the placenta. Transplacental infection of the fetus may occur and miscarriage, with or without invasion of the fetus, may result (Jones et al., 2000). In females that have been pregnant for up to 90 days, infection accounts for the occurrence of embryonic death, miscarriage, stillbirth and neonatal mortality (Dubey and Towle, 1986 and Barberan and Marco, 1997). The diagnosis of congenital toxoplasmosis can be performed by identifying the agent using histological slides and

the polymerase chain reaction (PCR) with aborted fetuses and placentas (Pereira-Bueno et al., 2004). The aim of this research was to study the contribution of T. gondii to reproductive failure using nested PCR and histopathological examination of fetuses, stillborns and placentas from naturally occurring miscarriages in sheep in the State of Pernambuco, Brazil. All experiments met or exceeded the standards set by the International Guiding Principles for Biomedical Research Involving Animals and all protocols were approved by the Federal Rural University of Pernambuco’s Ethical Committee (CEUA-UFRPE, protocol # 021-2009). Two hundred and forty-five organs and 28 placentas from 35 fetuses and stillborns from sheep raised in farms in the State of Pernambuco, Cell press Brazil, were obtained from naturally occurring miscarriages which were brought under refrigeration to the Federal Rural University of Pernambuco’s Infectious Diseases Laboratory. Pathological examination of the fetuses and the collection of samples were carried out according to the procedures outlined by Pérez et al. (2003). Fragments of brain, cerebellum, medulla, lung, heart, spleen, liver and placenta were collected for the nested PCR and histopathological examinations. The histological techniques used were those described by Prophet et al. (1992). Histological findings were classified as absent, unrelated lesions, consistent with or peculiar to toxoplasmosis.

Moreover, the space of alternative algorithms is vague because industrial algorithms are not typically published, “new” object recognition algorithms from the academic community appear every few months, and there is little incentive to produce algorithms this website as downloadable, well-documented code. Visual psychophysicists have traditionally worked in highly restricted stimulus domains and with tasks that are thought to provide cleaner inference about the internal workings of the visual system. There is little incentive to systematically

benchmark real-world object recognition performance for consumption by computational or experimental laboratories. Fortunately, we are seeing increasing calls for meaningful collaboration by funding agencies, and collaborative groups are now working on all three pieces of the problem: (1) collecting the relevant Kinase Inhibitor Library cell assay psychophysical data, (2) collecting the relevant neuroscience data, and (3) putting together large numbers of alternative, instantiated computational models (algorithms) that work on real images (e.g., Cadieu et al., 2007, Zoccolan et al.,

2007 and Pinto et al., 2009b, 2010; Majaj et al., 2012). We do not yet fully know how the brain solves object recognition. The first step is to clearly define the question itself. “Core object recognition,” the ability to rapidly recognize objects in the central visual field in the face of image variation, is a problem that, if solved, will be the cornerstone for understanding biological DNA ligase object recognition. Although systematic characterizations of behavior are still ongoing, the brain has already revealed its likely

solution to this problem in the spiking patterns of IT populations. Human-like levels of performance do not appear to require extensive recurrent communication, attention, task dependency, or complex coding schemes that incorporate precise spike timing or synchrony. Instead, experimental and theoretical results remain consistent with this parsimonious hypothesis: a largely feedforward, reflexively computed, cascaded scheme in which visual information is gradually transformed and retransmitted via a firing rate code along the ventral visual pathway, and presented for easy downstream consumption (i.e., simple weighted sums read out from the distributed population response). To understand how the brain computes this solution, we must consider the problem at different levels of abstraction and the links between those levels. At the neuronal population level, the population activity patterns in early sensory structures that correspond to different objects are tangled together, but they are gradually untangled as information is re-represented along the ventral stream and in IT.