5) ( Figures 2C and 2D) In addition,

5) ( Figures 2C and 2D). In addition, buy Erastin sex, age, or education covariates did not explain a significant proportion of variance in any of the reversal error scores (R2 < 0.01, F(3,678) < 1.8; p > 0.1). In summary, the present data set reveals a double dissociation between effects of the SERT and DAT1 genotypes on reversal learning, with SERT altering global lose-shifting and DAT1 altering postreversal perseveration. In a final ANOVA, we ascertained that the relative difference in lose-shift and perseveration Z scores was predicted by the difference in SERT and DAT1 genotype (R2 = 0.16, F(5,676) < 25.5; p = 0.009). This significant interaction confirms

the double dissociation between the two effects, with SERT affecting lose-shifting but not perseveration, and DAT1 affecting perseveration but not lose-shifting. We http://www.selleck.co.jp/products/tenofovir-alafenamide-gs-7340.html next used computational models to investigate the mechanisms that might underlie the DAT1 genotype results. Although DAT1 shows robust effects in our data set, the measure of perseveration to which it is related is relatively opaque, in contrast to the more direct measure of trial-by-trial switching with which SERT was associated. This opaqueness results from the fact that (perseveration) error scores require some form of “topdown” definition or knowledge by the experimenter, e.g., when the reversal, unbeknownst to the subject, has occurred. This has hampered comparison

of previous studies of reversal learning studies, which have reported a veritable zoo of reversal error measures, such as errors to criterion, total reversal errors, maintenance errors, perseverative errors, learning errors, and chance errors. Models of reinforcement learning can provide a more principled approach to assessing behavior, because they are independent of such external definitions that the subject is unaware of (learning criterion, point of reversal). Instead, like for win-stay/lose-shift measures, they take into account only past choices and observed outcomes. We aimed

to understand the process or mechanism underlying the effect of DAT1 on perseveration using a reinforcement learning model to examine how perseveration Etomidate can arise from a learning process integrating reward over a longer timescale. For simplicity, we do not consider the more transparent SERT effects on lose-shift behavior here, although we have verified in simulations not reported here that our model captures them when it is augmented with an additional parameter that directly controls switching after losses, without affecting long-term value integration. In the context of reinforcement learning models, two features of the DAT1 effects are puzzling. First, the effect is selective to the reversal phase, and second, the relationship between performance in the acquisition and reversal phases reverses sign depending on genotype.

In line with this prediction, the typical NMDAR-dependent LTP of

In line with this prediction, the typical NMDAR-dependent LTP of AMPARs is also absent after cocaine (Argilli et al., 2008, Luu and Malenka, 2008 and Mameli et al., 2011), probably due to a change in NMDARs that are no longer able to induce plasticity. The observation that targeted deletion of GluN3A abolished the cocaine-driven NMDA subunit redistribution indicates that GluN3A is necessary for the expression of cocaine-evoked plasticity of both AMPAR- and NMDAR-mediated

transmission. A critical step will be to understand the role for GluN3 in behavioral changes triggered by cocaine experience. Previous studies have explored the link between cocaine-evoked plasticity and addiction-relevant behaviors Paclitaxel solubility dmso (Engblom et al., 2008 and Mameli et al., 2009). Notably, deletion of the GluN1 subunit specifically in dopamine neurons, using a NR1 floxed x DAT cre mouse line, was found to impair reinstatement of cocaine seeking in both conditioned place BYL719 in vivo preference and drug self-administration paradigms (Engblom et al., 2008, Zweifel et al., 2008 and Mameli et al., 2009). In light of our findings, one possibility is that impaired reinstatement was due in part to a loss of GluN3-containing NMDAR subunits in VTA neurons. Although we saw no differences in both behavioral sensitization to cocaine and CPP using an ShRNA approach, we might predict that GluN3A plays an important role in the ability of cocaine-associated

stimuli to trigger relapse to drug seeking. The tight coupling of NMDAR and AMPAR redistribution also raises the possibility that at other synapses, where GluA2-lacking AMPARs have been observed, the NMDA transmission may be affected. For example, CP-AMPARs are present at excitatory synapses

onto interneurons in the cortex and hippocampus (Liu and Zukin, 2007). In these cells, an anti-Hebbian form of LTP that is induced by Ca2+ entering the cells through AMPARs can be observed (Lamsa et al., 2007). Whether Ca2+-impermeable NMDAR are also present at these synapses has not been investigated. As described above, both CP-AMPARs and GluN3A-containing NMDARs are present at many synapses during the early postnatal development (Ho et al., 2007, Henson et al., 2010 and Bellone et al., 2011) and may be permissive for circuit formation in Urease the developing brain and for activity-dependent changes in the mature brain. Regardless of the identity of the molecular linker, the subunit switch for NMDARs and AMPARs represents a form of metaplasticity. Rather than encoding specific events, cocaine sets the rules for subsequent activity-dependent synaptic plasticity (Mameli et al., 2011). After cocaine, NMDAR activation no longer induces LTP (because of the insignificant Ca2+ permeability), which, however, can be rescued when hyperpolarizing the cell during the induction protocol (thus favoring Ca2+ entry via GluA2-lacking inwardly rectifiying AMPARs).

The genetic correlations for the frontal pole seed point displaye

The genetic correlations for the frontal pole seed point displayed a clear A-P division, with a boundary separating positive and negative genetic correlations approximately PLX3397 chemical structure aligned with the central sulcus (see Figure S1 available

online for anatomical location), a border between motor and sensory areas (Figure 1A). The positive genetic correlations in Figure 1A show that genetic factors associated with expansion of the surface area around the seed point (indicated by a black dot) are also associated with expansion of other frontal regions (indicated by the red-to-yellow color scale). The negative genetic correlations in the posterior regions show that genetic influences associated with areal expansion of the frontal pole seed region cause relative areal contraction in posterior regions (indicated by the blue-to-cyan color scale). Findings from several mouse studies using experimental inhibition or overexpression of specific genes support the antagonistic A-P genetic effects. For instance,

the transcription factor Pax6 has anterior-high to posterior-low gradients of gene expression and promotes frontal/motor areal expansion (Bishop et al., 2000). Another transcription factor, Emx2, is expressed in an opposite gradient (Bishop et al., 2000 and Mallamaci et al., 2000). Furthermore, Pax6 and Emx2 mutually suppress MK 2206 one another’s expression, regulating areal expansion. In addition to the A-P division described above (Figure 1A),

positive genetic correlations were observed around the S1 seed region in the primary sensory and superior parietal cortices and partially in the primary motor cortex (Figure 1B). Genetic correlations with S1 resulted in a primarily postcentral division, with correlations becoming negative anterior to the precentral sulcus and roughly posterior and inferior to the parietal lobe. Area patterning for the anterior temporal pole seed point showed positive genetic correlations primarily in the temporal lobes, including the presumed human homolog of mouse A1, with negative genetic correlations in the rostral and caudal regions (Figure 1C). For the V1 seed region, we observed strong positive genetic correlations covering the occipital cortex. The correlations extended partially to the superior Oxygenase parietal cortex, which was suggestive of the dorsal stream of the visual system (Kandel et al., 2000). Genetic correlations with the V1 seed region were negative for anterior temporal and frontal cortices (Figure 1D). The boundaries of the genetic correlations corresponded substantially to known anatomical landmarks (e.g., major sulci such as the central sulcus). However, some boundaries did not match any traditional anatomical divisions. The observed patterns may reflect the combinatory actions of many other molecular gradients, including D-V and medial-lateral gradients in addition to A-P gradients.

molgen ua ac be/ADMutations) FAD-linked PS mutations cause neomo

molgen.ua.ac.be/ADMutations). FAD-linked PS mutations cause neomorphic protease activity, leading to increased production of Aβ42, the more Ruxolitinib ic50 hydrophobic and aggregation-prone peptides, compared to Aβ40 ( Figure 3A) ( De Strooper and Annaert, 2010). The prevailing amyloid hypothesis posits that accumulation of Aβ42 peptides triggers a pathogenic cascade, leading to neurodegeneration ( Hardy and Higgins, 1992). Therefore, it is thought that inhibition of γ-secretase activity may help to lower Aβ production serving as a therapy for AD. This therapeutic approach is tempered by the finding that conditional inactivation of PS1/2 in the adult mouse brain

causes progressive memory loss check details and neurodegeneration ( Saura et al., 2004 and Zhang et al., 2009), raising the possibility that γ-secretase activity is required for maintaining normal brain function ( Shen and Kelleher, 2007). Notch and APP represent only two examples of an expanding list of γ-secretase substrates that are known to undergo sequential proteolytic cleavage. Although this list includes many axon guidance molecules, the functional consequences of γ-secretase cleavage are best defined for the Netrin receptor DCC (Table 1). The extracellular

domain of DCC is first cleaved by a metalloprotease to create a membrane-tethered DCC stub. Under normal conditions the DCC stub is present at low concentrations because it is rapidly cleaved by γ-secretase, releasing the intracellular domain (ICD) from the membrane (Figure 3C). In vitro studies have shown that inhibition of γ-secretase activity results in accumulation of DCC stubs in cell membranes and is correlated with enhanced neurite outgrowth in cultured neuroblastoma cells (Figure 3E) (Parent et al., 2005 and Taniguchi et al., 2003). Although PS1 and PS2 mutant mice have been studied for more than a decade, the in vivo function of γ-secretase cleavage of guidance

molecules such as DCC was uncertain, perhaps because of the diversity of PS functions ( Donoviel et al., 1999 and Shen et al., 1997). A role for PS1 in axon guidance was first revealed in a mouse ENU mutagenesis screen to identify genes involved in embryonic motor neuron axon pathfinding ( Bai et al., Endonuclease 2011). Bai and colleagues discovered that motor axons in the Columbus mutant grew into the spinal cord floor plate at the midline rather than exiting laterally through their normal ventral root sites and found that this phenotype is caused by a mutation in the PS1 gene. Through a series of in vivo and in vitro experiments they linked this axon guidance phenotype to a defect in γ-secretase processing of DCC, causing motor neurons to inappropriately become attracted to the Netrin-1 produced by the floor plate ( Bai et al., 2011).

An electrode positioned close to the ventral nerve cord was used

An electrode positioned close to the ventral nerve cord was used to stimulate evoked release by applying a 0.5 ms 85 μA square pulse with a stimulus current generator (WPI). Further analysis www.selleckchem.com/products/ABT-263.html was done with IGOR Pro (WaveMetrics). Illumination was provided with a Sutter Instrument Lambda LS with a filter wheel for shuttering. The excitation light was filtered with 480 nm excitation filter (N41012; Chroma) and

focused on the specimen with a 63× water immersion objective (Olympus). Light intensity measurement was done similarly to that described for cell culture recordings. Cultured cortical neurons (15 DIV) plated on a glass-bottom culture dish were imaged on a Zeiss Live 5 Confocal Microscope with a 20× air objective. The neurons were electroporated with the indicated plasmids prior to

plating. Prior to imaging, the cells were treated briefly with balanced saline solution containing 40 mM selleck KCl before placed in the same external solution used in cell culture recordings. Five to seven regions (318 μm × 318 μm) on each dish were tested per experiment. After acquiring the initial image of eGFP/Citrine fluorescence of each region, a quadrant of the field of view (159 μm × 159 μm) was scanned with 488 nm laser (25% of 100 mW) with pixel dwelling time of 154 μs for 90 frames, given each pixel the cumulative illumination time of 13.86 ms. The sample was then perfused for 2.5 min (∼3.5 ml) of 40 mM KCl containing-external solution containing 10 μM FM4-64FX (Life Technologies) before washout with standard external solution with no FM4-64 for 7.5 min (∼10 ml). The same regions were then re-imaged for FM4-64 fluorescence. The eGFP/citrine fluorescence was excited with 488 nm laser (5% intensity of 100 mW) and imaged with a 505 LP emission filter and pixel dwell time of 154 μs. The FM4-64 fluorescence was excited with 532 nm laser (10% of intensity of 75 mW) and imaged with a 650 LP emission filter (pixel dwell time of 131 μs). For both imaging

and CALI, 5 optical slices with 0.84 μm spacing were acquired in the z series. For the analysis of the results, the CALI regions were identified on the images and the FM4-64 fluorescence of the puncta inside and outside the CALI region were quantified separately. tuclazepam As not all eGFP or Citrine positive puncta are presynaptic boutons capable of vesicular release (Figure S1), only puncta positive for both eGFP/Citrine and FM4-64 were used for quantification to avoid false negative. However, this criterion also underestimates the inhibition of vesicular release with InSynC, as presynaptic boutons that were strongly inhibited and failed to take up FM4-64 were not quantified. The mean fluorescence value from a region with no fluorescent structures in the FM4-64 image was chosen to provide the background value to be substracted. The fluorescence values were measured on ImageJ.

It has a corresponding property in intermediate level vision, tha

It has a corresponding property in intermediate level vision, that of contour integration. Even in V1, neurons’ responses show selectivity for the properties of extended contours with complex geometries. Neurons’ responses are greatly facilitated by collinear interactions, where a line placed outside the RF, which by itself will elicit no response, can facilitate a neuron’s response several-fold

selleck inhibitor when placed in conjunction with a collinear line segment within the RF (Figure 2; Kapadia et al., 1995, 2000). Blocking the continuity between line segments by a perpendicular line will eliminate the facilitation, but moving the perpendicular line segment into a different depth plane than the two collinear line segments, which restores their perceived continuity, recovers the facilitatory interaction of the collinear lines on neurons’ responses (Bakin et al., 2000). The properties of natural scene contours, the perceptual strategies by which we link contour elements, and the contextual interactions seen in V1 RFs are represented by the intrinsic circuitry of V1. An important feature of V1 connections is the plexus of long-range horizontal connections, which enable neurons to integrate inputs from an area of cortex representing an area of visual

field that is much larger than their classical RFs. The extent and orientation dependence of long-range horizontal connections match the properties of salient contours and the geometry of natural scene contours (Figure 3; Gilbert and Wiesel, 1989; Stettler et al., 2002; Li and Gilbert, ADP ribosylation factor click here 2002). By the same token, the visual system contains an internal representation of these principles, as observed in psychophysical studies of contour saliency (Field et al., 1993; Li and Gilbert,

2002), in facilitatory contextual influences on neuronal responses in V1 (Kapadia et al., 2000; Li et al., 2006; McManus et al., 2011) and in the long-range horizontal connections (Gilbert and Wiesel, 1989; Stettler et al., 2002). Together, these findings support the idea that the association field is represented in V1, and that the circuitry underlying lateral interactions in V1 mediates the linkage of scene elements into global contours. The horizontal connections play a role in experience-dependent plasticity. Such plasticity is invoked in the normal process of perceptual learning and in recovery of function following CNS damage, such as that associated with stroke or neurodegenerative disease. Even in adult animals, the adult visual cortex is capable of undergoing experience-dependent change. A valuable model for studying the mechanism of cortical plasticity at the levels of RF properties, changes in circuitry and molecular mechanism involve the reorganization of cortical topography following retinal lesions (Calford et al., 2000; Chino et al., 1992; Eysel et al., 1999; Giannikopoulos and Eysel, 2006; Gilbert et al.

NLG1 predominantly partitions to and regulates glutamatergic syna

NLG1 predominantly partitions to and regulates glutamatergic synapses (Chubykin et al., 2007; Graf et al., 2004). selleck screening library The loss of NLGs from PSD95-positive sites prompted us to test whether depolarization depletes NLG1 from the postsynaptic density (PSD). Due to the lack of NLG1-specific antibodies suitable for immunocytochemistry, we performed biochemical fractionation of DIV21 cortical cultures after KCl stimulation (Ehlers, 2003) and measured NLG1 levels using an antibody targeted against the extracellular N-terminal domain. Immunoblot analysis of isolated fractions revealed enrichment of NLG1 in the PSD (Figure S1

available online). KCl depolarization resulted in a significant loss (47.6% ± 1.8%) of NLG1 from total extracts (Figures 1C and 1D). This reduction in NLG1 was observed in both synaptic plasma membrane (SPM) and PSD fractions (30.5% ± 1.5% decrease in SPM; 23.9% ± 7.3% in PSDI; 45.1% ± 5.4% in PSDIII) and was particularly pronounced in Triton-insoluble PSDII fractions (72.9% ± 4.9% reduction), in which NLG1 is most highly enriched (Figure S1). We next tested whether KCl incubation increases NLG1 internalization and lysosomal degradation using surface biotinylation (Ehlers, 2000). To inhibit lysosomal proteolysis, cells were preincubated with leupeptin for 1 hr. In basal conditions, 5.3% ±

1.2% of surface NLG1 was internalized Gamma-secretase inhibitor over 2 hr (Figures 1E and 1F). This low internalization rate was unaltered by KCl (5.7% ± 0.8% of surface NLG1 internalized), indicating that KCl-induced NLG1 loss is not due to increased internalization. By contrast, the GluA1 receptor exhibited a marked increase in old internalization upon KCl stimulation (Figure 1F, right panel), similar to previous reports (Ehlers, 2000). We further

addressed whether KCl-induced loss of total NLG1 was sensitive to proteasome or lysosome inhibition. Incubation with KCl for 2 hr resulted in a 48.1% ± 2.6% reduction of total NLG1 levels, which was unaffected by proteasome inhibition (MG132, 50 μM), blockade of lysosomal degradation (leupeptin, 200 μM), or both together (MG132, 51.5% ± 5.7%; leupeptin, 46.3% ± 6.7%; both, 47.4% ± 4.2% of control; Figures 1G and 1H). However, incubation with the broad-spectrum MMP inhibitor GM6001 (10 μM) abolished KCl-induced loss of NLG1 (102.9 ± 1.1% of control; Figures 1G and 1H), whereas incubation with GM6001, MG132, or leupeptin alone did not significantly alter NLG1 levels under basal conditions (MG132, 103.6% ± 4.4%; leupeptin, 102.1% ± 0.8%; GM6001, 109.8% ± 5.1% of control; Figures S1B and S1C). To test whether NLG1 is cleaved at the plasma membrane, we developed an assay based on surface biotinylation (Figure 2A). Briefly, DIV21 neuronal cultures were covalently labeled with cell impermeable biotin (Sulfo-LC-Biotin-NHS, 1 mg/ml) to exclusively label surface proteins.

Despite the fact that layer 2/3 pyramidal neurons have been consi

Despite the fact that layer 2/3 pyramidal neurons have been considered to be a relatively homogeneous cell population, it is well established that in vivo firing rates among these cells can vary more than ten-fold. Similarly, it has long been noted that a subset of neurons in the neocortex exhibit expression of the activity-dependent gene c-fos even under basal conditions. Here we show that a history of immediate-early gene expression is an indicator of elevated spontaneous firing activity in a subpopulation of layer 2/3 pyramidal neurons. Whether elevated activity is a cause or an effect of activated IEG expression,

these data indicate that some neurons disproportionately contribute to the propagation of neocortical activity. It has recently been proposed Temsirolimus research buy that a single extra

spike within a neocortical neuron might be capable of driving dozens of spikes in its synaptically connected partners ( London et al., 2010), and indeed, under some conditions stimulation of a single neurons can alter global network activity ( Li et al., 2009) and perception ( Houweling and Brecht, 2008). Based upon this finding, we propose that fosGFP+ neurons may Selleckchem PLX-4720 drive or propagate network activity and information transfer across brain areas. Is sensory input required to drive fosGFP expression and indirectly, the increased spontaneous firing activity of these cells? Our preliminary analysis

suggests this is not the case. Bilateral removal of all large facial vibrissae for 24 hr did not eliminate or even noticeably reduce fosGFP expression in layer 2/3. In addition, paired-cell recordings showed that fosGFP+ cells maintained elevated firing activity in sensory-deprived tissue (data not shown). Although it is possible that whisker removal is not sufficient to get rid of all afferent activity, these data suggest that sensory input is not required for fosGFP expression or elevated spontaneous firing. The question of whether these cell assemblies are generated from internal neocortical dynamics or are constructed by information from the periphery (Kenet et al., 2003, MacLean et al., 2005 and Golshani TCL et al., 2009) is of great interest. It has been suggested that the population of neurons exhibiting both high and low levels of activity are unstable and drift over timescales ranging from seconds to minutes (Ikegaya et al., 2004, Kerr et al., 2007 and Mokeichev et al., 2007). Our data indicate that the firing output of a cell is much more conserved than previously estimated. Due to the time course of fosGFP expression, which requires at least 2–3 hr to become fluorescently visible, we conclude that a subpopulation of neurons exhibits specific network connectivity, driving elevated activity that can be maintained for at least 4–7 hr.

To investigate the morphology and projections of these excited ne

To investigate the morphology and projections of these excited neurons, we combined sharp electrode recordings with intracellular labeling of individual neurons. Our observations revealed that OT-excited neurons were localized in the CeL, whereas AVP-excited cells were found in the CeM. Subsequent tracing studies showed that the axon collaterals

of the OT-excited cells projected far into the CeM, and immunohistochemical staining showed that they were GABAergic. Further whole-cell patch-clamp recordings indeed showed that the inhibitory effects of OT were related with a massive increase of inhibitory GABAergic currents, induced by the activation of the CeL neurons (Huber et al., 2005). The above set of results led us to the development of a model in which the opposing behavioral effects of AVP and OT are PD-1/PD-L1 targets caused by a Autophagy Compound Library selective activation of two distinct populations: GABAergic neurons in the CeL are activated by OT and project to the CeM, where they exert inhibitory effects on neurons that are directly activated by AVP receptors (Figure 4B). OTergic modulation of the inhibitory projection from the CeL onto the CeM can therefore control the input to the CeL and the subsequent output from the CeM (Huber et al., 2005). Of potential interest in this context, it deserves mentioning that both the ventral CA1 and subiculum send direct projections to

the CeA, especially its capsular part (Cenquizca and Swanson, 2007), which may have the potential to mediate the ventral hippocampal contribution to fear learning (see below). With the aforementioned

homology between the CeA and the BSTl and their high levels of adjacent, nonoverlapping OTR and V1aR binding sites (Veinante and Freund-Mercier, 1997; Figure 4A), the question arises whether opposite effects of OT/AVP can also be found in the BSTl? Though no effects of V1aR activation seem to have been reported yet, strong excitatory effects of OT have been reported (Wilson et al., 2005). Similar to the desensitization differences between the CeA and MeA (Terenzi and Ingram, 2005; ALOX15 see above), OT effects in the BSTl showed faster desensitization compared to the BSTma. Both the CeA and BSTl are reciprocally connected to brainstem centers, particularly the dorsal vagal complex and parabrachial nucleus (Gray and Magnuson, 1987; Moga et al., 1989), and it is possible that OT action in these nuclei is involved in modulating autonomic functions. The nucleus of the solitary tract (NTS) is the major visceral sensory relay nucleus in the brainstem and receives signals from arterial baroreceptors, chemoreceptors, cardiopulmonary receptors, and other visceral receptors in an “organ-topic” manner through inputs from the solitary tract (ST). It is heavily innervated by the CeA and projects back to among others the CeL, as well as to the dorsal motor nucleus of the vagus (DMN) and the rostral ventrolateral medulla (RVLM, Figures 4D and 4E).

As expected, in relation to developmental stage, the level of pro

As expected, in relation to developmental stage, the level of protection in the TcCa group was different from that in the BSA group (p < 0.0001, Chi-square = 16). These results indicate a significant association

between each immunogen and the stage of parasite development. The influence of immunisation on the Modulators cysticerci development was verified when the length or diameter of cysts was measured after classification (Fig. 3). Because of the high variation between parasite dimensions, they were separated into 3 groups: ≤1 mm, 1< x < 5 mm, and ≥5 mm. The coupled peptide and the crude antigen induced resistance in mice and Hydroxychloroquine research buy similarly prevented an increase in the size of the parasites when compared with control group. On the other hand, although NC-1/BSA immunised mice had a smaller number of larval cysticerci,

animals exhibited a more pronounced number of ≤1 mm cysticerci than TcCa group (p < 0.005, Student's test) meaning active reproduction. These results indicate that NC-1/BSA was not as efficient as TcCa in inhibiting budding. Mice serum containing antibodies produced against the synthetic mimotope NC-1/BSA, TcCa, and BSA were used to immunolocalise native protein(s) in metacestodes of T. crassiceps. We performed an indirect immunofluorescence on the larval and final stages of the parasite. Immunofluorescence staining of mouse anti-NC-1/BSA antibodies on the T. crassiceps larval stage showed that the reactive protein(s) was present in the tegument this website of the cysticerci and, lightly, in the

parenchyma. The immunoreaction occurred mainly on the surface of the tegument ( Fig. 4I). Different reactivity occurred in response to the internal tissues with TcCa antibodies; although the labelling was predominantly tegument staining, proteins from parenchyma cells were also significantly reactive ( Fig. 4H). The reactivity profile changed when sections of the final stage of the metacestode were used. The immunofluorescence displayed after using antibodies produced against not TcCa was homogeneous on both parenchyma and tegument (Fig. 5H). This homogeneity was also verified when anti-NC-1/BSA antibodies were assayed, but curiously, an intense staining pattern of all tissue components of the section occurred as well (Fig. 5I). As expected, no reactivity was detected in sections incubated with mouse anti-BSA antibodies used as a negative control when tested on either the larval (see Fig. 3G) or the final stage of the developing parasite (see Fig. 4G). We have shown that NC-1 (SKSSITITNKRLTRK) can identify human neurocysticercosis on ELISA because it was selected using phage display by antibodies produced against T. solium antigens.