To minimize confusion between what is mental and what is physiolo

To minimize confusion between what is mental and what is physiological, we use the term “neural coordination” to refer specifically to the physiological coordination of neural activity, and we use the term “cognitive coordination” DAPT solubility dmso to refer to interpretations of behavioral observations. The experiments presented here were also formulated within the framework of the discoordination hypothesis, which asserts that disruption of neural coordination produces abnormalities in cognitive coordination, resulting in the core cognitive dysfunctions of schizophrenia.

This physiological hypothesis is agnostic to etiology of the disease and to whether there are abnormalities in dopaminergic, glutamatergic, GABAergic, or other neurotransmitter systems. It is thus remarkable that abnormal synchrony between the two hippocampi was associated with cognitive control difficulties in the adult NVHL rats and that the adolescent cognitive training corrected both the neural and cognitive abnormalities, which confirmed basic predictions of the discoordination hypothesis. We conclude that the present work offers an experimental platform for evaluating both the neurodevelopmental

and discoordination hypotheses. An important next step is to use the platform to evaluate other neurodevelopmental schizophrenia models with distinct Selleck ABT 263 etiologies such as the drug-induced methylazoxymethanol (MAM) model (Chen and Hillman,

1986; Featherstone et al., 2007), the polyriboinosinic-polyribocytidilic acid (PolyI:C) immune challenge model (Meyer et al., 2005; Pearce, 2001), and genetic models, such as the DISC1 (Kim et al., 2012) and other mutant mouse models (Belforte et al., 2010; Sigurdsson et al., 2010). The benefits Ketanserin of early cognitive training demonstrated in the NVHL model indicate the possibility of a critical window for procognitive intervention in schizophrenia and related disorders. This offers preclinical support for the idea that it is more effective to treat schizophrenia patients in the prodrome of the disease, at the very earliest signs of a disorder (Bird et al., 2010; Lieberman et al., 2001; Perkins et al., 2005). In fact, the present findings suggest that there may be substantial merit to explore the effectiveness of behavioral interventions even earlier in a preemptive effort. While further work in animal models will be needed to define and possibly expand (Maya Vetencourt et al., 2008) the boundaries of the opportunity, adolescence may be a natural target since it is characterized by substantial brain maturation (Shen et al., 2010; Uhlhaas et al., 2009; Yurgelun-Todd, 2007). The mechanism for the increase of interhippocampal synchrony we observed in the adolescent-trained NVHL rats is unknown and may be multifaceted.

Most diagnostic studies with multivoxel pattern analysis (MVPA) h

Most diagnostic studies with multivoxel pattern analysis (MVPA) have been based on structural imaging and some have obtained classification check details accuracies around 90% (Table 3). Although at such levels of accuracy, MVPA analysis of structural scans may in principle aid clinical diagnosis, accurately classifying psychiatric disease in patients suffering manifest clinical symptoms is perhaps not the greatest challenge of psychiatry. A real clinical benefit might be derived from the early detection of cases at high risk and the prediction of natural history

and treatment outcome. Koutsouleris et al. (2009) tested patients with prodromal symptoms of schizophrenia and obtained classification accuracies over 80% with whole-brain gray matter patterns between controls, early and late psychosis-risk states, as well as prediction of conversion to psychotic

disorder. The effectiveness of medication in preventing psychiatric disease even in psychologically well-defined high-risk groups (such as prodromal patients for schizophrenia or MCI for AD) is still not proven, and a better prediction of conversion risk through imaging would greatly aid clinical trials aimed at developing drugs that could be administered prophylactically in individuals with the highest risk. The prediction accuracies obtained this website by Koutsouleris et al. (2009) were in the upper range of those reported for purely clinical predictors (Klosterkötter et al., 2011), but a formal evaluation whether imaging biomarkers provide added value to clinical and psychometric predictors of psychosis is still lacking. Gray matter

volumetry is not the only parameter that has been utilized for such diagnostic and predictive purposes. Using DTI, Ingalhalikar et al. (2010) obtained high classification accuracy for schizophrenia in adults and for ASD in children. Similarly, Rathi et al. (2010) applied this method for early detection of first episode psychosis in schizophrenia. fMRI has also been used, particularly in depression, both during the resting state (Craddock et al., 2009) and during presentation of emotional facial expressions (Fu et al., 2008). Although the classification accuracy of MVPA techniques has been high in several studies, they may not reveal much about the underlying neurobiology of Levetiracetam the disorder. The mutual dependence of signal from different voxels often prevents simple neuroanatomical interpretations. However, the feature maps may provide some indication of which neuroanatomical correlates are particularly relevant for the diagnosis in question. For example, the patients with fragile X syndrome (FXS) showed a distinctive pattern of volume increases (basal ganglia) and decreases (frontal lobe) (Hoeft et al., 2008), and the late prodromal group showed relative gray matter decrease in many cortical areas but also increases in other areas including the thalamus (Koutsouleris et al.

g , (Carta et al , 2013, Park et al , 2004 and Petrini et al , 20

g., (Carta et al., 2013, Park et al., 2004 and Petrini et al., 2009)) up to ex vivo brain slices (e.g., (Bellone and Nicoll, 2007, Makino and Malinow, 2009, Mameli et al., 2007 and Shi et al., 1999)) and even in vivo (Brown et al., 2010, Rao-Ruiz et al., 2011 and Rumpel et al., 2005). Altogether, data from many labs favor

a three-step mechanism for the regulation of AMPAR numbers at synaptic sites during LTP involving exocytosis at extra/perisynaptic sites, lateral diffusion to synapses and a subsequent rate-limiting diffusional trapping step (Opazo and Choquet, 2011). Conversely, LTD has been proposed to involve lateral diffusion out of synapses, see more followed by endocytosis at extra/perisynaptic sites (Groc and Choquet, 2006 and Newpher and Ehlers, 2009) (Figure 3C). These different trafficking steps are regulated during synaptic plasticity and their detailed description is beyond the scope of 3MA this review. As a representative example, changes in the synaptic accumulation of AMPARs at synapses have been suggested to be a major substrate for NMDAR dependent LTP (Choquet, 2010, Kennedy and Ehlers, 2006, Lisman et al., 2007 and Shepherd and Huganir, 2007). LTP at CA1 synapses in the hippocampus is initiated by the influx of Ca2+ through NMDAR into dendritic spines. The synaptic increase in AMPAR number at synapses is likely to

be a multistep process including their exocytosis from endosomes those to extrasynaptic membranes (Kennedy et al., 2010 and Yudowski et al., 2006), lateral diffusion of receptors into the synapse, and their subsequent trapping. The relative timing of AMPAR exocytosis during LTP is still ambiguous, and we and others (Makino and Malinow,

2009, Opazo and Choquet, 2011, Opazo et al., 2010 and Tomita et al., 2005) have proposed that synaptic trapping of pre-existing surface receptors through rapid (sub-second) CaMKII induced phosphorylation of TARPs is the first event of potentiation. Regulated exocytosis of AMPARs occurs on a slower (tens of seconds) time scale and recruits other signaling pathways that may involve the ras-ERK pathway (Patterson et al., 2010) and Band 4.1 (Lin et al., 2009). Similarly, plasticity of inhibitory synapses involves regulation of the traffic of GABA(A)Rs or GlyRs (reviewed in Luscher et al., 2011 and Ribrault et al., 2011b) by activity-dependent and cell-type-specific changes in exocytosis, endocytic recycling, diffusion dynamics, and degradation of receptors. As for the glutamate receptors, these regulatory mechanisms involve receptor-interacting proteins, scaffold proteins, synaptic adhesion proteins, and enzymes (Figure 3A). For example, neuronal activity modifies diffusion properties of GABA(A)Rs in cultured hippocampal neurons (Bannai et al., 2009).

From the kinetic information obtained for isolated PSCs, the form

From the kinetic information obtained for isolated PSCs, the former are expected to be steeper even when several time-shifted PSCs overlap. The values of the derivative at such extremal points are shown as cumulative histograms in Figures 4B and 6D. We found that for our data, FFT does selleckchem not allow quantitative statements on the fast structure of cPSCs because of their short duration and the disproportionate weight assigned to events with higher-amplitude oscillations. Also, the temporal fine structure differs from event to event. This variability

is particularly problematic for analyses in the frequency domain, as for high frequencies f a small temporal jitter Δt is transformed to a large frequency jitter Δf = −f2/Δt PFT�� order owing to the reciprocal relation f = 1/t. To quantify the rhythmicity of fast network input during cPSCs, we instead analyzed the intervals between strong slopes within cPSCs ( Figure 4C: 10% strongest interdownward slope intervals in red, 25% strongest in gray; 0.5–400 Hz trace; see also Figures 6E and

S4B). The ripple band peak is robust for a wide range of low-pass frequencies (400–600 Hz) and fractions of selected strongest slopes (1%–25%). Filtering out higher frequencies is required to avoid too many local extrema of the derivatives being detected for what is in practice

the same onset. EPSCs outside SWRs (“spontaneous PSCs”) were detected among the cells Ketanserin recorded at −66 mV as strong downward slopes (top 5% of all maximal slopes on the 0.5–400 Hz filtered intracellular trace of each cell). A total of 1,000 events from 5 cells were postselected by eye to exclude those that are too small to be distinguished from noise and also to avoid multiple events where a second PSC arrives during the tail of the first. The fit was performed with an alpha function α(t;A,t0,τd,τr)=AN(τd,τr)Θ(t−t0)[e−(t−t0)τd−e−(t−t0)τr],where N(τd,τr) is a normalization factor so that the fitted amplitude A corresponds to the maximum value attained by the function, and Θ(t-t0) is the Heaviside step function defined as 1 for positive arguments (t later than onset t0) and 0 elsewhere. The average time constants obtained from the fits were of τr = 1.70 ± 0.04 ms and τd = 4.04 ± 0.08 ms. Here our PSC detection algorithm is based on slopes that are influenced by both time constants. To highlight the separation of timescales used by the algorithm, we plot histograms of durations of rises and decays (20%–80% and 80%–20% of maximum amplitude) instead of time constants ( Figure 4A).

Each host was infested with 25 pairs (adults) of R sanguineus T

Each host was infested with 25 pairs (adults) of R. sanguineus. The food was offered to hosts on the day of infestation, which was performed

according to methodology proposed by Bechara et al. (1995). Procedures performed in this study were approved by the ethics committee from OTX015 mouse UNESP Comitê de Ética no Uso de Animal (CEUA) Protocol 006/2009. After complete engorgement of R. sanguineus females and their voluntary detachment from the host, they were anesthetized by thermal shock in refrigerator, dissected and had their ovaries removed. The organs were fixed according to the techniques applied, and then dehydrated in increasing ethanol concentrations (70, 80, 90 and 95%) for 15 min each. After dehydration, the material was soaked in historesin (Leica) for 24 h, embedded and 3 μm

sections were made, which were collected on glass slides for subsequent staining. The ovaries were fixed in calcium–formaldehyde for 2 h. After collection on glass slides, they remained for 18 h in calcium dichromate, being subsequently washed in distilled water. The slides remained for 5 h in a hematein solution. Shortly afterwards, a second and last wash in distilled water was carried out. Once dried, Luminespib in vitro the slides were mounted with glycerin and coated with a coverslip. The photo-documentation was performed with a Motic BA 300 photomicroscope on the day the technique was completed to prevent discoloration (Baker, 1946). According to Pearse (1985), the material was fixed in 4% paraformaldehyde for 2 h and the glass slides containing the histological sections were stained with bromophenol blue for 2 h, at room temperature. After this period, they from were washed with 0.5% acetic acid for 5 min and with running water for 15 min. Then, they were quickly immersed in tertiary butyl alcohol and left to dry at room temperature for subsequent mounting in Canada balsam. Afterwards, the histological sections were photographed with a Motic BA 300 photomicroscope. Initially, the material was

fixed in aqueous Bouin’s solution for 12 h and the histological sections were rehydrated for 1 min in distilled water. The material was then stained with 1% Alcian blue in 3% acetic acid for 30 min and washed in distilled water. The sections were transferred to 1% periodic acid solution for 5 min and washed for 10 min in distilled water. After 15 min in Schiff reagent, the material was washed again for 7 min in running water. After drying, the slides were mounted in Canada balsam to be later observed and photographed with a Motic BA 300 photomicroscope (McManus, 1946 and Junqueira and Junqueira, 1983). The histological sections of the ovaries show a larger amount of oocytes in more advanced development stages in CG individuals (Fig. 1A) when compared to TG individuals (Fig. 1G). However, a stronger positive staining for lipids in oocytes I from the TG (Fig. 1H) than those from the CG is observed (Fig. 1B).

19 Thus it would appear that body temperature responses to differ

19 Thus it would appear that body temperature responses to differing light intensities can vary greatly, and with such an inconsistent response it is not easy to assign changes in body temperature as the cause for the differences in muscle endurance. The negative effect that melatonin (either endogenous or exogenous) has upon mental alertness and function might also explain the decrease in work performance. Dollins et al.20 found that melatonin (1, 20, 40, or 80 mg) significantly decreased the number GS-7340 manufacturer of correct responses in auditory vigilance, response latency in reaction time, and self-reported vigor. This

group also found that melatonin increased self-reported fatigue, confusion, and sleepiness. Using a similar testing protocol, Atkinson et al.5 found that 5 mg melatonin reduced alertness and short-term memory. In addition, eight-choice reaction time was slower at different times of day after ingesting melatonin, but exogenous melatonin did not influence

perceived exertion. On the other hand, Atkinson and associates19 found selleckchem that 2.5 mg melatonin had no effect upon mental alertness of perceived exertion before or after exercise. The above responses to melatonin would suggest that melatonin could dull the drive need to perform continual lifts, and some researchers have found confirming relationships when comparing dark and bright light exposure. For instance, French et al.14 found individuals exposed to 3000 lx had higher mental capacities than when they were exposed to 100 lx. On the other hand, Saulov and Lufi21 found no difference in perceived effort, energy,

tiredness, pleasure, and satisfaction after exercising in either normal light or dim light. Unfortunately, these researchers did not quantify the light intensity levels of their two conditions.21 Finally, Ohkuwa et al.10 measured plasma epinephrine after either 5000 lx or and 50 lx exposure for 90 min and found that epinephrine was significantly lower after bright light exposure than after dim light exposure. It is difficult to ascribe the lower work output seen in this study to a reduced neural drive when dim light shows higher epinephrine levels. A third mechanism that could relate to improved work following bright light exposure relates to changes in blood flow. Aizawa and Tokura13 found that blood flow Sitaxentan increased faster with increasing temperature during almost 11.5 h of exposure in 4000 lx vs. 100 lx. Kim and Jeong 17 also found that forearm skin blood flow tended to remain steady in 700 lx, but decreased markedly in 70 lx. Melatonin supplementation, however, shows differing responses to what would be expected from dark induced endogenous melatonin production. Atkinson et al. 19 found that during exercise, 2.5 mg melatonin magnified the increase in skin blood flow. Cook et al. 22 found that 3 mg melatonin supplementation had differing influences across various vascular beds.

, 1998) Therefore, it is possible that extracellular concentrati

, 1998). Therefore, it is possible that extracellular concentrations of endogenous DBI peptides in discrete areas such as nRT are at a lower level that is more likely to exert PAM rather than NAM effects. In contrast to the stark nRT versus VB differences in physiological PAM effects of DBI, immunoreactivity to DBI was observed in both nRT selleck kinase inhibitor and VB (Figure 5). In this regard, it is important to note that DBI is also known as ACBP and the Dbi/Acbp gene is thought to ubiquitously serve housekeeping functions ( Knudsen et al., 1993), generating

an intracellular protein critically involved in facilitating intracellular transport of Acyl-CoA. We hypothesize that the nRT versus

VB differences in the electrophysiological findings likely represent nucleus-specific differences in the extracellular release and processing of DBI. In the current studies, we used a viral strategy to examine whether Dbi gene products are necessary and sufficient to produce endozepine actions in nRT. Although it is possible that viral introduction of DBI into a system in this way induces changes in its modulatory effects, it is unlikely that this explains the PAM actions observed here, as a recent report using similar viral vectors to express DBI and ODN GW786034 clinical trial in the SVZ exclusively observed NAM effects ( Alfonso et al., 2012). The mechanism(s) underlying these differences remain to be determined, though one possible explanation is differential intra- or extracellular processing of DBI, the nature of which is specific to certain areas or cell types. It is certainly

conceivable that some DBI fragments exert PAM effects, whereas others are NAMs. In addition, preliminary evidence suggests that exogenous application of DBI does not alter sIPSCs in VB (C.A.C. and unless J.R.H., unpublished data), in contrast to the robust potentiation of uncaging responses when VB sniffer patches are placed in nRT. This further supports a working model in which nRT-specific processing of Dbi gene products underlies the PAM actions. Strikingly, endogenous BZ-mimicking potentiation was observed in nRT, but not in adjacent VB thalamus. This raises the question of why such effects would be specifically localized to nRT, and not VB. Perhaps selection pressure led to evolution of an adaptive specific subcircuit modulation in nRT that reduces the possibility of seizure occurrence. Synaptic inhibition in nRT exerts a prominent desynchronizing effect to reduce the propensity for oscillatory activity (von Krosigk et al., 1993; Huntsman et al., 1999; Schofield et al., 2009), and potentiation of synaptic inhibition by BZs further suppresses oscillations (Huguenard and Prince, 1994a; Sohal and Huguenard, 2003; Sohal et al., 2003).

To distinguish whether directional selectivity

in the pre

To distinguish whether directional selectivity

in the presence of inhibitory blockers arose pre- or postsynaptically, the properties of ganglion cell light-evoked synaptic inputs were analyzed using whole-cell voltage-clamp techniques. In these experiments, after measuring spikes in cell-attached mode in the presence of blockers (Figure 6A), the same cell was patched with an electrode containing intracellular solution. After PD-1/PD-L1 inhibitor drugs break-in, the DSGC was dialyzed with QX314 and Cs+ and repeatedly injected with brief depolarizing pulses (−60–0 mV) until Na+ currents and a large fraction of voltage-gated K+ currents were blocked. Under these conditions, moving spots elicited large inward currents in both the null and preferred directions (VHOLD = −60 mV; Figure 6B). When the cell was held ∼0 mV, the inhibitory inputs that are usually associated with stimulating these cells (Figures 3A and S3) were not apparent, confirming that they were effectively blocked with the cocktail of antagonists (also see Figure S4). At +40 mV, light evoked outward currents. Importantly, the

temporal characteristics of currents measured at −60 and +40 mV were similar (Figure S5), indicating that they were not contaminated by voltage-dependent conductances, and thus provided a reliable readout of bipolar cell output. Reversal of the excitatory currents also indicated that gap junctions did not significantly contribute to the synaptic responses (Ackert et al., Selleck Antidiabetic Compound Library 2009). Under conditions in which inhibitory receptors and active postsynaptic conductances were blocked, preferred and null-direction stimuli evoked excitatory currents that were similar in size. The amplitude of the peak currents was not significantly different

whether measured at −60 mV (preferred: −228 ± 30 pA and −136 ± Adenylyl cyclase 24 pA, for ON and OFF, respectively; null: −206 ± 30 pA and −131 ± 18 pA for ON and OFF, respectively; p > 0.6; n = 6) or +40 mV (preferred: 353 ± 64 pA and 214 ± 44 pA, for ON and OFF, respectively; null: 373 ± 67 pA and 216 ± 40 pA for ON and OFF, respectively; p > 0.6; n = 6; Figure 6C). Similarly, the total charge of the response was similar in magnitude in the null and preferred directions, indicating that moving spots stimulated an equal number of inputs in both directions (−60 mV ON, −113 ± 18 nC for preferred compared to −126 ± 21 nC for null; −60 mV OFF, −54 ± 13 nC for preferred compared to −66 ± 16 nC for null; +40 mV ON, 227 ± 52 nC for preferred compared to 265 ± 54 nC for null; +40 mV OFF, 124 ± 26 nC for preferred compared to 141 ± 29 nC for null; p > 0.5; n = 6; Figure 6D). The symmetry in input strength contrasts with the asymmetry in the spiking responses and suggests that nonlinearities within the ganglion cell must contribute to direction discrimination.

The reliability of these measurements

The reliability of these measurements Veliparib order that were established in this laboratory was less than 6% for the CV. A Shapiro–Wilk test was used to confirm that all dependent variables were normally distributed. The changes in the muscle damage markers, leukocytes and CD34+ cells, and hematocrit over time after the first eccentric exercise were analyzed by a one-way

repeated measures ANOVA, followed by a Tukey’s post hoc test when a significant time effect was found to locate the time points that were different from the baseline values. To compare between the first and second sessions for changes in muscle damage markers, leukocytes and CD34+ cells, and hematocrit, a two-way repeated measures ANOVA was used. When a significant session × time interaction effect was observed, a Tukey’s post hoc test was performed

to compare the first and second sessions for each time point separately. All analyses were conducted with SPSS software (version 17.0, SPSS Inc., Chicago, IL, USA), and a p < 0.05 was considered statistically significant. The results were presented as means ± SD. The changes in MVC torque, muscle soreness, and plasma CK activity are shown in Table 1. After the first eccentric exercise session, the MVC torque decreased more than 50% immediately and 24 h post-exercise, and did not recover to the baseline by 96 h post-exercise. Muscle soreness developed after the exercise, and peaked at 48–72 h post-exercise. These changes after the first session were similar between click here the entire subject group (n = 9) and those subjects in the sub-group (n = 6) who performed the

second eccentric exercise session 4 weeks later. After the second exercise session, the MVC torque recovered significantly faster to the baseline, and the muscle soreness was significantly less as compared with the first session. No significant changes in plasma L-NAME HCl CK activity were evident after the first session because of the large variability in the responses among subjects. However, all subjects showed increases from the baseline (peak–baseline value = 155–3562 IU/L). No significant changes in plasma CK activity were evident after the second session. No significant changes in hematocrit were observed over time, and the average value was 0.44 ± 0.02. Changes in the number of total leukocytes, neutrophils, lymphocytes, monocytes, and eosinophils are shown in Fig. 1. No significant changes in the number of any cells were observed after the first and second eccentric exercise sessions. The number of CD34+ cells per mL of blood ranged from 1400 to 7000 (average 3200 ± 1497) at baseline. No significant changes in this number were evident over time for both sessions, and no significant differences in the changes were evident between sessions. As shown in Fig. 2, no significant changes in the percentage of CD34+ cells to the total number of leukocyte cells were evident either after exercise.

Pairs of V4 and FEF sites with overlapping RFs showed gamma-band

Pairs of V4 and FEF sites with overlapping RFs showed gamma-band coherence that was enhanced when attention was inside the joint RF (Gregoriou et al., 2009). Long-range gamma-band coherence has also been studied with noninvasive recordings in human subjects (Schoffelen et al., 2005, 2011; Siegel et al., 2008; Hipp et al., 2011). For example, Schoffelen et al. showed that corticospinal gamma-band coherence indexes a subject’s dynamic movement preparation (Schoffelen et al., 2005) selectively among those corticospinal neurons involved in the upcoming movement (Schoffelen et al., 2011). To study interareal coherence

between monkey areas V1 and V4, we have relied on electrocorticographic LFP recordings that measure the electrical activity under the electrode. Neither the volume of tissue nor the way in see more which it affects the recording are fully understood. Yet, a few statements about ECoG recordings can be made. (1) ECoG signals do not provide a direct measure of spiking activity, and, therefore, our results do not directly test predictions that might be derived from the CTC hypothesis about spike synchronization. (2) ECoG recordings from V1 reflect both V1 neurons with connections to V4 and other V1 neurons. Similarly,

ECoG recordings from V4 reflect V4 neurons with direct input from V1 and other V4 neurons. Therefore, our results do not directly DAPT quantify the coherence between V1 output neurons and their postsynaptic target neurons in V4. Such an analysis would have required the simultaneous recording of interareal pairs of isolated single units, identified to be monosynaptically coupled to each other. While this would have been technically extremely challenging, it would at the same time have rendered the analysis of interareal coherence extremely insensitive. Isolated 4-Aminobutyrate aminotransferase single neurons reflect with their sparse spiking only poorly the phase of the underlying rhythm. For two isolated single neurons in V1 and V4, coherence analysis would have been exceedingly insensitive (Zeitler et al., 2006). (3) ECoG recordings combine spatial resolution in the range of few millimeters

(Figure 1C) with excellent sensitivity for the rhythms in the respective local neuronal population (Figure 1B). The core prediction of the CTC hypothesis with regard to selective attention relates to this mesoscopic level: the V4 rhythm is selectively coherent with the V1 rhythm that is driven by the behaviorally relevant stimulus. To test this prediction, simultaneous multiarea ECoG recordings are ideal. Spike recordings in V4 would have allowed testing whether postsynaptic neurons responded primarily to the attended stimulus. However, this core result from the attention field (Moran and Desimone, 1985; Reynolds et al., 1999) has been replicated several times and presumably holds also in our experiment. Thereby, our present results actually also support the “Binding by Synchronization” (BBS) hypothesis.