01). Subsequent two-way repeated-measures anovas of error rates on pro- or anti-saccade trials revealed that the three-way interaction was due to a greater influence of cue direction on pro-saccade vs. anti-saccades, and time of stimulation of anti-saccade vs. pro-saccade trials. The filled symbols in Fig. 3A and B and the histograms learn more in Fig. 3C and D give a sense of the consistency in these changes across the sample, and permit a comparison of the magnitude of changes in RT across different tasks and directions.

In particular, note the robustness of the increases in bilateral anti-saccade RT for stimulation times in the post-cue interval (increases were observed in the vast majority of sessions). We also represent the RTs of anti-saccade errors in Fig. 3. The RTs of anti-saccade errors

always exceeded 200 ms, even for the latest stimulation time, emphasizing again that ICMS-SEF is neither driving saccades directly nor evoking express saccades. Note also how the RTs for ipsilateral anti-saccade errors are longer than the RTs for ipsilateral pro-saccades for later stimulation times (Fig. 3B). This observation is relevant to the potential influence of ICMS-SEF on anti-saccade performance, and will be returned to in the Discussion. To summarize, short-duration ICMS-SEF OSI-906 influenced both the error rates and the RTs of pro- and anti-saccades. This influence is characterized by strong dependencies with both the task, with error rates and RTs increasing Clomifene for anti-saccades, and the time of stimulation, with greater influences emerging the later stimulation is passed relative to cue onset. Importantly, the observation of a greater influence of ICMS-SEF on saccades in anti- vs. pro-saccades alleviates concerns about the animals anticipating the delivery of stimulation, given that half of our stimulation times occur after cue onset. If the animals were being distracted by the increasing possibility of ICMS-SEF as the trial progressed, such distraction may have been manifest in a similar ways on pro- and anti-saccade

trials, which differs from what we observed. Furthermore, although we did observe some asymmetries with saccade direction, short-duration ICMS-SEF increases the error rate and RT of both ipsilaterally and contralaterally directed anti-saccades. We now describe the effect of short-duration ICMS-SEF on neck muscle recruitment, focusing first on the recruitment evoked bilaterally on muscles involved in horizontal head turns, and then on how we have quantified such evoked recruitment. The data in Fig. 4A are taken from a single representative session, and show neck muscle recruitment aligned to stimulation onset collapsed across all experimental conditions. As with longer duration ICMS-SEF (Chapman et al.

The loxP recombination sites are only 34 bp in length and Cre will recombine essentially any DNA substrates that contain these sites, with no requirements for the accessory proteins (Abremski & Hoess, 1985; Abremski et al., 1986). However, introducing loxP AZD6244 sites into pathogenic E. coli genomes using the common existing techniques has the disadvantage of being time-consuming (Murphy & Campellone, 2003; Lee et al., 2009). A

simple mutagenesis method without DNA cloning has been developed in E. coli. This method depends on the lambda Red gam, bet, and exo gene products, which encode an efficient homologs recombination system (Datsenko & Wanner, 2000; Yu et al., 2000). Using this method, modifications can be targeted precisely and can range from single base-pair deletions or insertions to the addition or deletion of sequences in the kilobase-pair range. Selection for the positive phenotype of the introduced

mutation has been difficult to achieve, making the use of a counter-selection approach very useful for the mutagenesis (Reyrat et al., 1998). A powerful counter-selection system for the introduction of mutations based on the wild-type rpsL gene responsible for streptomycin sensitivity has been described (Zhang et al., 2003; Rivero-Müller et al., 2007; Heermann et al., 2008). In E. coli, the rpsL gene encodes selleckchem the S12 ribosomal protein of the 30S subunit, which is the target of streptomycin. Streptomycin inhibits protein, synthesis by binding near the interface of S12 ribosomal Adenosine protein, hence increasing the translational errors (Karimi & Ehrenberg, 1994, 1996). The prerequisite for this system to be effective is streptomycin-resistant strain. Resistance because of chromosomal mutations within rpsL is recessive in a merodiploid strain (Reyrat et al., 1998; Gill & Amyes, 2004). When both wild-type and mutant alleles of rpsL are expressed in the same strain, the strain

becomes sensitive to streptomycin (Reyrat et al., 1998). Here a method for site-directed mutagenesis of the APEC chromosome is described. Lambda Red recombination is used to introduce the loxP sites flanking the rpsL-neo marker into the APEC genome, and the Cre/lox system is used to remove the marker. Further, it is shown that rpsL counter-selection is applicable for introducing modifications into the APEC genome. Strains used and generated in this study are listed in Table 1. APEC1 strain was isolated from an infected chicken (Vandemaele et al., 2003). APEC1 strains containing plasmid pKD46 (Table 1) responsible for the homologs recombination (Datsenko & Wanner, 2000) and plasmid pSC101-BAD-Cre-tet (Anastassiadis et al., 2009) containing the cre gene responsible for the recombination of the loxP sites were incubated at 30 °C unless otherwise mentioned.

5 min). This is the first indication of a significant difference in the oxidation state of the PQQ prosthetic group in the catalytic sites of the active and inactive ADHs, respectively. The pH-dependence profiles for the ferric reductase activities of the ADHa and ADHi complexes were compared (Fig. 4a). The ADHa complex showed its maximal activity at pH 6.0 with learn more small shoulders in the acidic and alkaline sides of the curve. On the other hand,

ADHi showed the maximal response at pH 4.5 without secondary responses in the alkaline and acidic sides of the slope. ADH possesses multiple cytochrome c centers, which are potentially reactive sites from which electrons can be withdrawn by the ferricyanide electron acceptor. The distinct optimal pH seen for ADHi suggests that ferricyanide reacts at a single site, other than that

preferentially used in the active and fully reduced ADHa. Thus, the pH profile of ADHi must be attributed to the electron donor activity of the cytochrome c in subunit I, which is based on the pH-dependence profiles previously obtained for the catalytic activity of the dissociated and partially reconstituted subunit complexes of the trimeric ADH complex of G. suboxydans (Matsushita et al., 1996) where the complex formed by subunits I and III (SI-SIII complex) showed a distinctive acidic optimal pH and very low activity, such as was shown by our inactive enzyme. In this regard, it must be remembered that SI bears the catalytic site and one of each, PQQ and cytochrome www.selleckchem.com/products/SB-431542.html c, whereas SII contains three cytochromes c and that in trimeric ADHs SIII click here does not seem to have a role in the catalytic process (Matsushita et al., 1994). On the other hand, our ADHa (Fig. 4a) and the native ADH complex from G. suboxydans exhibit their maximal response at mild alkaline conditions (Matsushita et al., 1989). The heme c components of the ADHi complex were redox titrated at pH 6.0. Titration was

monitored from 500 to 600 nm, following the change of the α-band maximum at 553 nm (reference wavelength set at 540 nm, dual wavelength mode). The best fit of the redox titration data for our enzyme (Fig. 4b) revealed the presence of four potentials at Em1 = −34 mV (20%), Em2 = +90 mV (18%), Em3 = +215 (26%), and Em4 = +270 mV (36%) (vs. SHE). These values are significantly more positive than the mid-potential values obtained previously for its active counterpart (10): −64 mV (31%), −8 mV (18%), +185 mV (30%), and +210 mV (13%) (vs. SHE, pH 6.0). ADH quinohemoproteins are complex enzymes carrying several redox prosthetic groups. Notably, the four cytochrome c centers are redox-dependent chromogenic groups amenable for the assessment of electron transfer kinetics within the ADH complex. Accordingly, the rate of intramolecular electron transfer evoked by ethanol was measured in both ADHi and ADHa.

In addition, each rat received an IP injection of saline 1 day before the induction phase of AMPH sensitization. Half of the rats were then administered a single daily AMPH (1 mg/kg IP) injection (sensitized group; SEN) and half were administered saline (non-sensitized group; NON) for four consecutive days while Z-VAD-FMK cell line locomotor activity was recorded (Robinson, 1984; Robinson & Becker, 1986). Spontaneous locomotor behaviour was monitored in activity chambers (Truscan Activity Monitoring System; Coulbourn Instruments, Allentown, PA, USA). Each chamber (39 × 42 × 50 cm) had four transparent Plexiglas walls and a removable plastic tray at the bottom. Chambers were placed in sound-attenuating boxes in a dark room.

Locomotor buy U0126 activity was monitored for a period of 120 min, by recording infrared beam interruptions on two sensor rings placed around the chambers (on the outside of the Plexiglas walls), creating a 16 × 16 beam matrix. The monitoring session was divided into pre-injection (30 min) and

post-injection (90 min) components, during which the truscan Software recorded total time spent moving. All rats were tested throughout the experiment in the same respective activity chamber at the same time of day. After a 1-week AMPH withdrawal period, rats were administered an initial AMPH challenge (0.5 mg/kg IP) to determine whether they exhibited sensitization to the locomotor stimulating effects of AMPH (see Fig. 1 for experimental timeline). The doses selected for the subsequent challenge injections were based on a pilot study, in PRKD3 which it was observed that AMPH doses > 0.25 mg/kg resulted in stereotypy (data not shown). As stated

previously, rats were divided into two main groups, SEN (n = 32) and NON (n = 32). Within each of these groups and following the initial AMPH challenge, rats were assigned to one of four E2 groups: SEN with low E2 replacement (n = 16), SEN with high E2 replacement (n = 16), NON with low E2 replacement (n = 16) and NON with high E2 replacement (n = 16). These groups were each then further divided into two conditions depending upon whether they received chronic HAL or chronic saline (SAL). The final group designations were as follows: sensitized, with high E2 replacement and HAL (HE; HE/SEN; n = 8), sensitized with high E2 replacement and SAL (SE; SE/SEN; n = 8), sensitized with low E2 replacement and HAL (He; He/SEN; n = 8), low E2 replacement and SAL (Se; Se/SEN; n = 8), non-sensitized with high E2 and HAL (HE/NON; n = 8), non-sensitized with high E2 and SAL (SE/NON; n = 8), non-sensitized with low E2 and HAL (He/NON; n = 8) and non-sensitized with low E2 and SAL (Se/NON; n = 8). Rats were administered four subsequent AMPH (0.25 mg/kg, IP) challenges on days 2, 10 and 12 of HAL or SAL treatment and 1 week after discontinuation of HAL treatment. Locomotor activity was assessed on days 2 and 12 in order to compare short- versus long-term HAL treatment.

For reason of clarity, we limited our analysis to genes induced ≥threefold and repressed ≥fivefold by rhamnolipids. Genes controlled by the same regulator form discrete clusters based on their expression pattern under different stress conditions (Fig. 2a). Genes belonging to the cell envelope stress response of B. subtilis are grouped in three clusters and can be assigned to two regulators, σM and the LiaRS TCS (Fig. 2b).

They are induced by cell wall antibiotics and rhamnolipids, but not by secretion stress (with the exception of liaH). One of these three clusters contains the target operon of the LiaRS TCS as well as the downstream genes gerAAAB. The other two clusters include mostly target genes of σM. Noteworthy, within the σM regulon, there is a subset of genes, including the mreBCDminCD operon involved in cell division, that is not induced by vancomycin (upper part of σM1 cluster in Fig. 2b). Differences in the induction learn more profiles of subsets of σM-dependent

genes have been observed previously (Eiamphungporn & Helmann, 2008). Genes mediating the secretion stress response also cluster together (Fig. 2b). The CssRS-dependent target genes htrA and htrB are SB431542 not only induced by secretion stress and rhamnolipids, but also weakly by vancomycin and bacitracin. Genes repressed by rhamnolipids show almost unchanged expression under the other conditions tested (Fig. 2c). One exception is the pyr operon, which is strongly repressed by rhamnolipids,

but weakly induced by friulimicin and vancomycin. Taken together, the hierarchical clustering analysis indicates that rhamnolipids induce a combination of two different stress responses: the cell envelope stress response represented by the LiaRS TCS and the ECF σ factor σM, and the heat and secretion stress response mediated by CssRS. Simultaneous induction of the LiaRS TCS and σM is common for cell wall antibiotics such as daptomycin, vancomycin, or bacitracin (Mascher et al., 2003; Hachmann et al., 2009; Wecke et al., 2009). But none of the σM-dependent target genes is induced by secretion stress, while both the CssRS and LiaRS TCS are induced by cell wall antibiotics, rhamnolipids, and secretion stress, but with different intensities Alanine-glyoxylate transaminase (Fig. 2d). Bacteria use signal transducing systems to detect harmful compounds and alter gene expression to protect the cell. We hypothesize that the signal transducing systems activated by rhamnolipids confer resistance and counteract cell damage caused by this antimicrobial compound. Therefore, we compared the growth behavior of B. subtilis wild-type cultures exposed to different rhamnolipid concentrations with strains carrying gene deletions leading to ‘ON’ or ‘OFF’ states of the induced signal transducing systems, which results either in no or constitutively high expression of the corresponding target genes.

Similar to what was observed in our present study, differential expression of TNF-α isoforms was demonstrated after stimulation with LPS or stimulation of the hemoparasite Trypanoplasma borreli, with a predominant rise in TNF-α2 (Zou et al., 2002; Bridle et al., 2006). Rainbow trout infected with the

protozoan parasites Tetracapsuloides brysalmonae mTOR inhibitor (the causative agent of proliferative kidney disease) and Neoparamoeba sp. (causative agent of amoebic gill disease) also displayed an increased expression of TNF-α2 relative to TNF-α1. In contrast, stimulation by IHN virus (causative agent of infectious hematopoietic necrosis) by the protozoan Ichthyophthirius multifiliis (‘white spot’ disease) or by the monogenean parasite Gyrodactylus derjavini

(skin fluke) induced an increase in the expression of the TNF-α1 isoform at a higher magnitude than that of the TNF-α2 isoform. check details Thus, the differential expression of TNF-α isoforms is apparently dependent on the species of pathogen or stimulus, the tissue sampled and the species of fish studied (Purcell et al., 2004; Bridle et al., 2006), and the results obtained here probably reflect the interaction of S. iniae EPS with different cell types, including granulocytes and nongranulocytes present in the blood and organs. Indeed, the use of an in vivo system may help to preserve the integrity of cellular interactions, as well as the effect of lymphocyte-derived factors on proinflammatory cytokine production and,

similarly to other studies, ensues in elevated cytokine levels (O’Dwyer et al., 2006; Bozza et al., 2007). The role of EPS in S. iniae pathogenesis is poorly understood. There is evidence, however, that the interaction between the immune system and the EPS produced by this pathogen play an important role in both the development of the disease and protection against the pathogen (Eyngor et al., 2008). Not surprisingly, it is now revealed that EPS is also a key molecule in S. iniae pathogenesis; the failure to control the inflammatory cascade following Non-specific serine/threonine protein kinase EPS administration is accompanied by a considerable increase in the secretion of proinflammatory cytokines that are likely to be at the origin of clinical manifestations and poor outcome, both of which are typical of septic shock. Indeed, several inflammatory and infectious diseases are associated with the overproduction of proinflammatory cytokines and chemokines, and the recruitment and activation of different leukocyte populations are a hallmark of acute inflammation (Saukkonen et al., 1990; Welbourn & Young, 1992). These cytokines are believed to mediate responses associated with clinical deterioration, multiorgan system failure and death from septic shock (Waage et al., 1991; Anderson et al., 1992; Bone et al., 1992; Beutler & Grau, 1993; Bone, 1993; Casey et al.

Similar to what was observed in our present study, differential expression of TNF-α isoforms was demonstrated after stimulation with LPS or stimulation of the hemoparasite Trypanoplasma borreli, with a predominant rise in TNF-α2 (Zou et al., 2002; Bridle et al., 2006). Rainbow trout infected with the

protozoan parasites Tetracapsuloides brysalmonae this website (the causative agent of proliferative kidney disease) and Neoparamoeba sp. (causative agent of amoebic gill disease) also displayed an increased expression of TNF-α2 relative to TNF-α1. In contrast, stimulation by IHN virus (causative agent of infectious hematopoietic necrosis) by the protozoan Ichthyophthirius multifiliis (‘white spot’ disease) or by the monogenean parasite Gyrodactylus derjavini

(skin fluke) induced an increase in the expression of the TNF-α1 isoform at a higher magnitude than that of the TNF-α2 isoform. see more Thus, the differential expression of TNF-α isoforms is apparently dependent on the species of pathogen or stimulus, the tissue sampled and the species of fish studied (Purcell et al., 2004; Bridle et al., 2006), and the results obtained here probably reflect the interaction of S. iniae EPS with different cell types, including granulocytes and nongranulocytes present in the blood and organs. Indeed, the use of an in vivo system may help to preserve the integrity of cellular interactions, as well as the effect of lymphocyte-derived factors on proinflammatory cytokine production and,

similarly to other studies, ensues in elevated cytokine levels (O’Dwyer et al., 2006; Bozza et al., 2007). The role of EPS in S. iniae pathogenesis is poorly understood. There is evidence, however, that the interaction between the immune system and the EPS produced by this pathogen play an important role in both the development of the disease and protection against the pathogen (Eyngor et al., 2008). Not surprisingly, it is now revealed that EPS is also a key molecule in S. iniae pathogenesis; the failure to control the inflammatory cascade following Selleck RG7420 EPS administration is accompanied by a considerable increase in the secretion of proinflammatory cytokines that are likely to be at the origin of clinical manifestations and poor outcome, both of which are typical of septic shock. Indeed, several inflammatory and infectious diseases are associated with the overproduction of proinflammatory cytokines and chemokines, and the recruitment and activation of different leukocyte populations are a hallmark of acute inflammation (Saukkonen et al., 1990; Welbourn & Young, 1992). These cytokines are believed to mediate responses associated with clinical deterioration, multiorgan system failure and death from septic shock (Waage et al., 1991; Anderson et al., 1992; Bone et al., 1992; Beutler & Grau, 1993; Bone, 1993; Casey et al.

SopA is expressed mainly at the early stages of infection. These results are consistent with data reported earlier (Drecktrah et al., 2005; Giacomodonato

et al., 2007; Patel et al., 2009) and indicate that the expression of SopB can be induced and maintained in vivo under environmental conditions different to those found in the intestinal milieu. In agreement, our in vitro experiments http://www.selleckchem.com/products/CP-690550.html showed that SopB can be expressed and secreted in growth conditions that resemble early and late intracellular niches (Fig. 1). Concurrently, we investigated the in vivo translocation of SopB in the cytosol of infected cells isolated from MLN during murine Salmonella infection. Gentamicin experiments revealed that 80% of bacteria recovered from MLN were intracellular. This result was confirmed by electron microscopy (data not shown). As shown in Fig. 3b (lane 2), Selleckchem Palbociclib translocation of SopB in infected cells recovered from MLN was evident for at least 24 h after animal infection coincident with the peak of expression (Fig. 3a). At later time points we were not able to detect SopB in the cytosol of infected cells. On the other hand, although SopA is expressed at day 1 (Fig. 3a, lane 1), it could not be detected in the eukaryotic cytosol of infected cells (Fig. 3b,

lane 6). Again, we observed that the dual effector SopD is translocated during the first 24 h after inoculation (Fig. 3b, lane 4). To the best of our knowledge, this is the first time that the translocation of Salmonella SPI-1 effector proteins has been assessed in vivo. Altogether, our results are consistent with those reported earlier showing that sopB continues to be transcribed and translated in vitro for many hours after bacterial internalization (Knodler et al., 2009). Our work acknowledges the significance of analyzing protein expression

and Florfenicol translocation, in vivo, in the context of bacteria–host interactions. For instance, attenuated Salmonella carrier vaccines have the potential to be used as delivery systems for foreign antigens from pathogens of viral, bacterial and parasitic origin (Everest et al., 1995). In this regard, Panthel et al. (2005) proposed SPI-1 and SPI-2 type III effector proteins as carrier molecules for heterologous antigens. Taking into account our results, SopB appears as an attractive carrier, potentially able to translocate heterologous antigens at different time points of the Salmonella infection cycle. Moreover, Nagarajan et al. (2009) have recently highlighted the importance of understanding the time and the compartment in which expression of SPI-1 and SPI-2 proteins occurs in selecting vaccine candidates; the authors proposed Salmonella Typhimurium sopB as a potential DNA vaccine.

Among these soluble factors is leukemia inhibitory factor (LIF), a cytokine that exerts pleiotropic effects on cell survival. Here, data show that LIF effectively reduced infarct volume, reduced white matter injury and improved functional outcomes

when administered to rats following permanent middle cerebral artery occlusion. To further explore downstream signaling, primary oligodendrocyte cultures were exposed to oxygen–glucose deprivation to mimic stroke conditions. LIF significantly reduced lactate dehydrogenase release from OLs, reduced superoxide dismutase activity and induced peroxiredoxin 4 (Prdx4) transcript. Additionally, the protective and antioxidant capacity of LIF was negated by both Akt inhibition and co-incubation with Prdx4-neutralising antibodies, establishing a role for the Akt signaling pathway and Prdx4-mediated Alpelisib antioxidation in LIF protection. “
“Selective attention helps process the myriad of information constantly touching our body. Both endogenous and exogenous

mechanisms are relied upon to effectively process this information; however, it is unclear how they relate in the sense of touch. In three tasks we contrasted endogenous and exogenous event-related potential (ERP) Y-27632 nmr and behavioural effects. Unilateral tactile cues were followed by a tactile target at the same or opposite hand. Clear behavioural effects showed facilitation of expected targets both when the cue predicted targets at the same (endogenous predictive task) and opposite hand (endogenous counter-predictive task), and these effects also correlated with ERP effects of endogenous attention. In an exogenous task, where the cue was non-informative, inhibition of return

(IOR) was observed. The electrophysiological results demonstrated early effects of exogenous attention followed by later endogenous attention modulations. These effects were independent in both the endogenous predictive and exogenous tasks. However, voluntarily directing attention away from a cued body part influenced the early exogenous marker (N80). This suggests that the two mechanisms are interdependent, at least when the task requires more demanding shifts of attention. The early marker of exogenous tactile attention, the N80, was not directly related to IOR, which Resveratrol may suggest that exogenous attention and IOR are not necessarily two sides of the same coin. This study adds valuable new insight into how we process and select information presented to our body, showing both independent and interdependent effects of endogenous and exogenous attention in touch. Our largest organ, the skin, is constantly bombarded with an endless stream of tactile information. Endogenous attention helps us focus on what information is relevant and to predict upcoming sensory events. On the other hand, when something touches our body unexpectedly (e.g. a mosquito on our ankle), we rely upon exogenous attention to process this new and unexpected information.

The normalized signal change at the driving ssVEP frequency was then evaluated by means of an omnibus mixed-model anova, with CS Type (CS+,CS–), Phase (Baseline, Conditioning, Extinction) and Stimulus (Luminance, Chromatic) as the within-subject factors and Tagging Frequency (14 Hz, 15 Hz) as the between-subjects factor. Rating data obtained after each experimental phase were submitted to the same statistical model. A CS Type × Phase interaction was deemed necessary for inferring

a conditioning effect and served as a prerequisite for conducting follow-up anovas. An alpha level of 0.05 (two-tailed) was employed for all analyses. Ratings of hedonic valence and emotional arousal collected after the end of each experimental phase demonstrated clear evidence of fear conditioning. Across reversal

GSK126 concentration frequencies and stimulus types, participants rated the CS+ as more unpleasant (i.e., Selleck Trichostatin A lower in hedonic valence) than the CS– solely during the acquisition phase [F1,25 = 35.90, P < 0.001,  = 0.59], resulting in a CS Type x Phase interaction [F2,50 = 19.32, P < 0.001,  = 0.44] in the overall model. No differences were observed during the habituation and extinction phases (all F < 2.52, all P > 0.12). In terms of emotional arousal (intensity), main effects of experimental Phase [F(2,48]  = 12.60, P < 0.001,  = 0.34] and of CS Type [F(1,24] = 32.08, P < 0.001,  = 0.57] were qualified by an interaction of CS Type × Phase [F(2,48] = 18.68, P < 0.001,  = 0.44]. This interaction reflected Pyruvate dehydrogenase lipoamide kinase isozyme 1 the absence of CS-related arousal effects during habituation (all F < 2.42, all P > 0.13) and extinction (al F < 2.71, all P > 0.10), and greater rated emotional arousal specifically in response to the CS+ during acquisition [F1,25 = 58.50, P < 0.001,  = 0.71]. Importantly, behavioral ratings were not affected by stimulus type.

Both stimuli evoked strong and reliable ssVEPs at the reversal frequency, with a pronounced posterior topographical maximum (see Fig. 3). Focusing on local ssVEP amplitude over a group of occipital sensors, we observed a significant three-way CS Type × Phase × Stimulus [F2,48 = 6.39, P = 0.003,  = 0.21] interaction. As there were no significant effects involving Tagging Frequency (all P > 0.103), this factor was dropped in subsequent analyses. As suggested in Fig. 4, the crucial CS Type × Phase interaction [F2,50 = 9.80, P < 0.001,  = 0.28] was observed for low-spatial-frequency luminance stimuli only (chromatic stimuli, CS Type × Phase F < 1, P > 0.77). We next conducted a series of follow-up anova contrasts on ssVEPs evoked by the low-spatial-frequency luminance Gabor patches in each experimental phase. These analyses confirmed the visual impression conveyed by Fig. 5; a CS+ specific enhancement at posterior sensors was observed during the conditioning [F1,25 = 6.25, P = 0.019,  = 0.