We observed the same effect when the whole S2 segment was substituted in GluK3/K2S2 and GluK2/K3S2 chimeric receptors (Figure 5E). Hence, in addition to its role in the zinc action on GluK3, D759 in GluK3 appears as a key residue to explain the specific desensitization properties of GluK3 as compared to GluK1 and GluK2. We searched for additional residues involved in the binding of zinc in the vicinity of D759. This residue is localized in the turn between helices J and K of

the GluK3 LBD (Venskutonytė et al., 2011), three residues downstream of a conserved histidine near the N terminus of helix K. This conserved histidine, together with D759, is a candidate for residues forming part of the zinc binding site for 3-MA mouse GluK3. To test this hypothesis, GluK3 H762 was replaced by an alanine. As expected, the facilitatory effect of zinc was turned to an inhibitory effect in GluK3(H762A) (peak amplitude 45% ± 6%, n = 5; p = 0.014; Figures 6D and 6F), strongly suggesting that H762 participates in the zinc binding site of GluK3 receptors. In addition, the desensitization kinetics of GluK3(H762A) was faster (τdes = 3.9 ± 0.1 ms, n = 5; p = 0.0009; Figure 6G) than for WT GluK3, ruling out an indirect effect of reduced

desensitization on the effect of zinc in this mutant. To obtain further insight into the zinc binding site on GluK3, three independent crystal structures Smad inhibitor were solved for the GluK3 LBD in the presence of zinc: two in a complex with glutamate, and one in

a complex with kainate (Table S2). The structure for the six GluK3 protomers in the glutamate complexes was similar to that reported recently by Venskutonytė et al. (2011) but with small variations in the extent of domain closure, from 25.3° to 23.4°, and larger cavity volumes (299 ± 6 Å3, mean ± SD, n = 6) than the value of 274 ± 4 Å3 reported previously, indicating that the LBD of GluK3 is more similar to GluK1 than GluK2, with cavity volumes of 305 and 255 Å3, respectively (Mayer, 2005). For the two protomers in the GluK3 kainate complex (Figure S1), domain closure was 90% and 70% of that induced by glutamate, indicating that the GluK3 LBD can adopt both more closed, and also more open, conformations than observed previously for the GluK3 kainate complex for Thalidomide which a value of 81% was reported by Venskutonytė et al. (2012). In the crystal forms reported here, the GluK3 protomers assemble as two different dimers, both of which diverge from the canonical arrangement found in full-length GluA2 (Sobolevsky et al., 2009). In the P2221 glutamate and P2221 kainate complexes, two GluK3 protomers are arranged head to tail such that helix D of subunit A packs against the N terminus of helix K in subunit B (Figure 7A). Crystallographic symmetry operations generate a second dimer, arranged in a head-to-head assembly but with a >20 Å lateral displacement of the two protomers such that helix J is packed against helix J of its symmetry mate (Figure S1C).

, 2007) so all of the potential presynaptic cells of a certain subtype can be probed, providing a comprehensive account of connectivity probability. HSP inhibitor cancer Exciting technological advances lie ahead. This technique would be made even more influential by the added functionality of measuring relative synaptic strengths. The net effect of a population of neurons depends heavily on the strengths of its connections and subtle gradients in the synaptic strength matrix can underlie starkly different network behaviors.

Here, the binary results of Fino and Yuste (2011) demonstrate the maximum possible connectivity in the network because very weakly connected interneurons may not be able to induce inhibitory responses in postsynaptic pyramidal cells during physiological states in vivo. Thus, only a subset of the existing dense connections of interneurons to a given pyramidal cell may serve to modulate pyramidal cell output and it would be very useful to have this information embedded in our maps of synaptic Z-VAD-FMK cost connectivity. Another useful extension of the present work would be to combine it with calcium imaging that would enable the rapid

identification of all neurons postsynaptic to an interneuron targeted with glutamate uncaging. By categorizing the subtypes of these postsynaptic neurons, for example by post hoc immunostaining (Kerlin et al., 2010), this method could potentially provide a remarkably complete map of inhibitory connections. Furthermore, combined

glutamate uncaging and calcium imaging would be useful for circuits with a high degree of recurrent connectivity such as layer 2/3 cortex as it would be advantageous to be able to rapidly examine bidirectionality of connections. The ever-increasing array of optical, genetic, and electrophysiological tools will allow comprehensive, high-resolution functional maps of synaptic connections for different cortical layers, cortical regions, and species to soon lie within our reach. “
“Primary cilia were definitively identified in the vertebrate nervous system several decades ago, principally using electron microscopy (EM). Reports of primary cilia extending from neuroepithelial found progenitor cells into the lumen of the neural tube (Duncan, 1957 and Sotelo and Trujillo-Cenoz, 1958) were followed by descriptions of primary cilia on neurons and glia (Dahl, 1963, Karlsson, 1966, Palay, 1960 and Peters et al., 1976), and by the early eighties the prevailing view was that virtually all neurons are ciliated (Wheatley, 1982). The elegant ultrastructure and broad distribution of the primary cilium captured attention, but its function in neural cells was unclear (Peters et al., 1976). Intense recent scrutiny of the primary cilium has elucidated many functions in the body and brain, and the consequences of defective cilia for human disease.

In this study, parents of 12–23 months old children with no or partial

immunization were interviewed about the reasons for failing to immunize or partially vaccinating their children. Thirty-six percent of parents living in urban and 26% in rural areas did not feel the need to vaccinate their children while approximately 25% parents did not know their children could be protected with vaccines. About 11% were unaware of where to get children immunized. The pattern of response however differed between urban and rural settings. The reasons cited for partial immunization comprised lack of knowledge about ‘what vaccines were needed’ and ‘when those were to be given’. On the other hand, ‘fear of side effects’ was one of the major reasons for ‘no’ immunization. buy AG-014699 The macro-social issues raised in the rotavirus vaccine debate in India were (a) sanitary

hygiene and access http://www.selleckchem.com/products/LBH-589.html to safe drinking water, (b) ‘tropical barriers’ to oral vaccines, and (c) physicians’ perceptions of vaccination. While physicians’ views can influence vaccine dispensation among the public, the other issues (such as microbiota of gastrointestinal tract in tropical countries) influence vaccine uptake at the gut-level. Some authors who favored rotavirus vaccine as the principal mode of intervention also recognized sanitation, hygiene, and safe water supply as effective prevention measures against diarrheal diseases caused by bacteria and parasites [38]. They did not assign much weight to the above measures for controlling rotavirus gastroenteritis due to the ubiquitous presence of the virus in the developing and developed world. However, others have pointed out that such infrastructural interventions might indeed be useful [12] and [39] to reduce all causes of diarrheal morbidity and mortality, including that caused by rotavirus. This conviction comes from the fact that the severity of rotavirus gastroenteritis is influenced by the presence of co-infections in the gut, which in turn, is linked with poor civic infrastructure such as water supply and sewerage systems. A national survey [40], conducted in 2009–2010 to identify the predictors of administration

and attitude about mafosfamide vaccines including rotavirus, revealed that only a tenth of pediatricians had been routinely administering rotavirus vaccines in India. Unfortunately, we could neither locate any Indian study on perception of mothers about rotavirus vaccine nor a public debate. Diversity of protection (homotypic vs heterotypic) conferred by live oral rotavirus vaccine(s) in Indian setting has been raised as an issue [12]. Since early days of detection, an enormous diversity has been exhibited by rotavirus in India [15], [17], [18] and [19]. A recent review from the subcontinent has revealed that the most common G (G1–G4) and P-types (P [4] and P [8]) globally, accounted for three-fourths of all strains in this region [41].

The discussants considered not only the various regulatory systems that govern animal care and use, but also the emergence of private party actions to intervene in the enforcement of regulations and the increasing use of freedom of information approaches, such as federal and state “sunshine” legislation in the United States, to seek information about animal care and use (Institute of Medicine, 2012). While not representing a total consensus of all the workshop’s

participants, some important messages emerged during the presentations and subsequent discussions. Key among these was the need for a strong regulatory and institutional compliance framework to ensure that the use of animals in research is ethically secure and legally sound and to provide confidence in public communication about, and defense of, the research. At the same time, delegates were concerned to Dabrafenib find more avoid placing unnecessary constraints on important neuroscience research. The scientific study of living organisms is critical if we are to understand both life on earth and the diseases and disorders that we cannot yet treat or prevent. Since all living organisms have a common origin and all vertebrates

share a large fraction of their genes and a wide range of cellular mechanisms, we have already learned a great deal about the principles of human biology and behavior from animal models and can hope to learn more. Moreover, advances in veterinary care also depend crucially on understanding gained from the study of animals. A common feature of animal research

legislation around the world is that animals may be used for some experimental procedures that would not be acceptable in humans. These include manipulation of the environment, the genetics, or the PAK6 bodies of the animals. Nevertheless, it must be appreciated that the use of animals in neuroscience research raises particularly sharp ethical issues. The fact that many harrowing disorders of the nervous system, such as dementias, Parkinson’s disease, and motor neuron disorders, are increasing in prevalence and are not adequately treatable heightens the potential benefits of such research. But for the same reasons, neuroscience research often involves the creation of such distressing conditions in animals, or the manipulation of their experience, in ways that highlight the potential ethical costs of animal research. As neuroscience research moves forward, there is likely to be a continuing reliance on animal models. This likelihood must not be concealed in discussions with politicians, the media, the public, or with groups that oppose animal use. But this should not preclude grasping opportunities to implement the 3Rs: indeed any continuing need to use animals simply raises the moral imperative to optimize welfare and to search for every way to reduce suffering.

4). Cells were post-fixed for 1 h in the dark with a solution containing 1% osmium tetroxide, 1.25% potassium ferrocyanide and 5 mM CaCl2, in 0.1 M sodium cacodylate buffer (pH 7.4). Samples were dehydrated with increasing concentrations Proteasome inhibitor of acetone, and then embedded in PolyBed (Polyscience

Inc., Warrington, PA, USA). Ultrathin sections were stained with uranyl acetate and lead citrate and then observed using a Zeiss 900 Electron Microscope (Carl Zeiss, Inc.). For detection of polysaccharide inclusions, ultrathin sections of samples prepared for transmission electron microscopy, as described above, were processed for cytochemical detection of carbohydrates (Thiéry, 1967). Tissue cysts were used as a positive control for amylopectin granules. Cysts were obtained from mice previously infected with T. gondii strain Me49 for at least 4 weeks, based on the protocol established by Freyre (1995). Ultrathin sections collected on 200-mesh gold grids were incubated in 1% periodic acid for 30 min, washed in distilled water and incubated with 1% thiosemicarbazide in 10% acetic acid for 72 h. Next, the sections were washed in 10%, 5% and 2% acetic acid and 3 times in distilled

water for 10 min. Afterwards, the sections were incubated for 30 min with 1% silver proteinate in the dark and washed abundantly in distilled water. For control assays, periodic acid was omitted. The sections were observed in a Jeol 1200 EX transmission electron microscope operating at 80 kV. For imunofluorescence assays, LLC-MK2 cells infected with tachyzoites at a ratio of 3:1 parasite/host cell were treated with compounds 1, 2 or 3 for 48 h. At the end of treatment, www.selleckchem.com/products/bmn-673.html infected cells were fixed in 3.7% freshly prepared formaldehyde, permeabilized with 0.5% Triton X-100 for 15 min and blocked with 3% bovine serum albumine in PBS pH 7.4 for 1 h at room temperature. Cells were then incubated for 1 h in the presence of Dolichos biflorus lectin conjugated with FITC (DBA-FITC) 10 μg/ml (Sigma–Aldrich Co., St. Louis, MO, USA). After lectin labeling, the coverslips were mounted

and observed in a no Zeiss Axioplan microscope using the fluorescein filters. The azasterols inhibited T. gondii proliferation with IC50 values in the micromolar range. Table 1 shows the in vitro anti-proliferative activity of the azasterols. Compound 3 was the most active, showing an IC50 at nanomolar range after 48 h. The anti-proliferative activity range of the new compounds (0.8–4.7 μM) was of the same order as that previously obtained by our group for 22,26-azasterol and 24,25-(R,S)-epiminolanosterol ( Dantas-Leite et al., 2004). These results confirm that azasterols can cause growth inhibition of T. gondii, across a variety of different structural types. Interestingly, compounds do not necessarily need to have a basic nitrogen as can be seen from compounds 2 and 3, which has implications for the mode of action. In order to investigate the selective effect of the azasterols against T.

, 2010 and Suto et al., 2005). In addition, some Semas can also function as receptors to elicit signals check details in reverse ( Yu et al., 2010), although how cis-binding can influence Plexin:Sema reverse signaling is still unclear. Thus, cis-interaction between receptors and ligands in axon guidance signaling is emerging as a mechanism complementary to trans-interactions allowing for an increased diversity and modulation of growth cone responses. In addition to their role in axon guidance, Ephs and ephrins have been implicated in a multitude of processes such as

glucose homeostasis, immune responses, angiogenesis, and cancer (Pasquale, 2008). Ephs and ephrins are coexpressed in β cells in the pancreas (Konstantinova et al., 2007), T- and B cells (Nakanishi et al., 2007 and Wu and Luo, 2005), and several types of cancer cells (Ireton and Chen, 2005, Noren and Pasquale, 2007 and Pasquale, 2010), but the significance of Eph/ephrin cis-interaction is still unclear. The imbalance of Eph/ephrin function may contribute to disease progression, for example, in melanoma cells coexpressing Ephs and ephrins, where diverse effects of bidirectional 5-Fluoracil ic50 trans-signaling on proliferation and/or metastasis have

been reported ( Noren et al., 2006 and Yang et al., 2006), with little understanding of the contribution of Eph/ephrin cis-interactions in this context. However, our insights into ephrin cis-attenuation of Eph signaling in motor axon guidance as well as studies in other

systems suggest that ligand mediated cis-attenuation of receptor function is a universal mechanism for not only augmenting the diversity of axon guidance responses but it also modulating other cell signaling responses. Fertilized chicken eggs (Couvoir Simetin) were incubated and staged according to standard protocols (Hamburger and Hamilton, 1951). Chick spinal cord electroporation of expression plasmids or siRNAs was performed at HH st. 18/19 as described (Kao et al., 2009, Luria et al., 2008 and Momose et al., 1999). SiRNA duplex oligonucleotides with 3′TT overhang were purified over MicroSpin G-25 columns (GE Healthcare) until in 10 mM Tris-Cl (Fisher Scientific), 1 mM EDTA (Invitrogen), and 20 mM NaCl (EMD Chemicals). GFP expression plasmid (1 μg/μl) was coelectroporated with the siRNA solution to label motor axons. SiRNA sequences (sense strand) are [ephrin-A5]siRNA, 1:1 mixture of GCCAGAAGAUAAGACCGAA and GCUAUGUUCUGUACAUGGU; [ephrin-B2]siRNA, 1:1 mixture of GGACAAGGAUUGGUACUAU and GCCUGGAAUUUCAGAAGAA; scrambled [ephrin-A5]siRNA, 1:1 mixture of GCCGAAAUAAGACCAGGAA and GCUUUGGUCCAUUAAUGGU; scrambled [ephrin-B2]siRNA, 1:1 mixture of GGAAGGAGGUUCAUACUAU and GCCUAAGACUUAAGGUGAA. Retrograde labeling of chick motor neurons using HRP (Roche) as tracers was performed as described (Kao et al., 2009).

17 The power of the stance phase head and tibia acceleration in the frequency domain was determined CHIR 99021 by calculating the power spectral density (PSD) using a square window. Examination of the acceleration signals collected over the entire stance phase follows the periodic assumptions of Fourier analysis and allows for examination of frequencies below 15 Hz.45 and 46 The PSD was performed on frequencies 0 to the Nyquist frequency (FN) and normalized to 1 Hz bins. 14 and 22 After binning, the PSD was normalized in order for the sum of the powers from 0 to FN to be

equal to the mean squared amplitude of the data in the time domain. Examining the PSD results revealed two primary peaks or local maxima for the tibial and head acceleration signal power in both RF and FF running that were outside of the lower (4–8 Hz) and higher (10–20 Hz)

ranges previously identified selleck products in the literature for RF running. 13, 14, 15 and 17 As a result, we expanded the lower and higher frequency ranges investigated to 3–8 Hz and 9–20 Hz, respectively, to more appropriately include the dominating frequency components of each footfall pattern. The frequency at which peak power occurred within the lower and higher frequency range of the tibial (TPFlow, TPFhigh) and head (HPFlow, HPFhigh) acceleration signal was determined. Signal power magnitude in the frequency domain was quantified by the integral of the signal power contained in the lower and higher frequency ranges in the tibial (TSMlow, TSMhigh) and head (HSMlow, HSMhigh) acceleration signals. 15 A transfer function has been previously used to determine the degree of shock attenuation in human running by calculating the ratio of each frequency bin between the tibial and head signal14, 15, 19 and 22 (i.e., the transmissibility of each frequency component21). The transfer function was calculated across all frequencies from 0 to FN to determine the degree of shock attenuation occurring between the tibia to the head by: Shockattenuation=10×log10(PSDhead/PSDtibia) For each frequency, the transfer function calculated the gain or attenuation, in decibels,

between the tibia and head signals. Positive values indicated a gain, or increase in signal strength, and negative Ketanserin values indicated attenuation, or decrease in signal strength. A gain in lower frequency components is typically a result of changes in head vertical velocity and voluntary segment motion during the stance phase whereas negative values indicate attenuation in signal power as the impact shock travels through the body.17 and 22 Shock attenuation magnitude was quantified by the integral of the transfer function result within the lower (ATTlow) and higher frequency ranges (ATThigh). For the lower and higher frequency ranges, tibial and head peak signal power and signal magnitude were averaged across all stance phases of each participant and then across group.

The YFP/CFP ratio showed correlation with the relatively large movement under this recording condition (data not shown). AVE and AVB coimaged showed out-of-phase profiles and negative correlation ( Figure 1F). The YFP/CFP value for AVE and AVB recording in each sample was normalized by mean and SD. Pearson’s correlation coefficient was determined by R. Under this recording condition, backward motion was hyperstimulated compared to standard

culturing conditions. For correlation analyses of the averaged YFP/CFP ratio change during transitions of directions, YFP/CFP ratios before and after ABT-263 concentration directional change were collected and normalized against the YFP/CFP value immediately before the directional change. Traces from nine AVA/AVE and 15 AVB recordings were used for correlation analysis in Figures 1D and 1E. For correlation analysis between AVE and AVB activity, seven AVE/AVB recordings were analyzed to obtain the data shown in Figure 1F. To compare the interneuron calcium

signals between wild-type and innexin see more mutant animals, we compared the averaged YFP/CFP ratio instead of ΔR/R. YFP/CFP ratio for each sample during 5 min was presented by raster plots. The averaged YFP/CFP value over 5 min of recording for each sample was considered a single data point and presented as scatter plots (Figure 6; Figures S3A, S3B, and S7). This is because neurons analyzed in this study showed relatively high-frequency activation, and we rarely observed the decline of the calcium level to the basal value. In this case, measuring ΔR/R probably leads to an inaccurate measurement of neuronal activity. Imaging of motoneurons was carried out with a protocol modified from the AVA and AVE single-neuron imaging method (Figure 2, Figure 4 and Figure 8; Figure S1D). We dropped 20 μl M9 buffer onto a 2% dried agarose pad, and ∼20 adult animals were placed in the liquid as spacers. Ten last-larval stage (L4) hpIs171 animals were placed in the buffer, covered by a coverslip, and imaged with a 63× objective. Neurons were identified

by their stereotypic anatomical organization. Most data presented in Figure 4 and Figure 8 were obtained by manually recentering the moving animals during the recording and scoring the forward, backward, and kinking motion manually based on the direction of the body-bend propagation. During later parts below of the study, we utilized an in-house-developed automated tracking software to recenter animals, which allowed the automated analysis of the directional movement, as well as correlation between calcium transients with directions and velocity (Figures 2A and 2B, bottom). Samples that show sustained forward or backward movement (Figure 4 and Figure 8), instead of frequent directional change (Figure S1D), were quantified for the mean calcium level in continuous directional movement (Figure 4 and Figure 8). Locomotion direction and calcium transients showed similar correlation pattern in both data sets.

To test this hypothesis, we measured the association of CaMKIIα mRNA with PABP in the hippocampus of WT and Paip2a−/− mice using a ribonucleoprotein

immunoprecipitation (RIP) assay with PABP antibody. The association of PABP with CaMKIIα mRNAs was increased after contextual training in both groups. However, the Fulvestrant increase was greater in Paip2a−/− mice as compared to WT mice ( Figure 6F). Taken together, our data demonstrate that, while translation of CaMKIIα mRNA is not altered in Paip2a−/− mice under basal conditions, contextual training of Paip2a−/− mice leads to enhanced CaMKIIα mRNA translation. This is consistent with previous studies showing that the CaMKIIα mRNA contains two cytoplasmic polyadenylation elements (CPEs), binds the CPE binding protein, and undergoes NMDA- and experience-dependent elongation of poly(A) tail at synapses ( Huang et al., 2002; Wu et al., 1998). Translational activation by newly formed poly(A) tail depends on PABP binding, which, in turn, is regulated by PAIP2A.

We next examined the enhancement of CaMKIIα mRNA translation in Paip2a−/− mice by using immunostaining. Previous studies reported Baf-A1 molecular weight that tetanic stimulation increases CaMKIIα levels in CA1 pyramidal cell dendrites of acute hippocampal slices as early as 5 min after the stimulation in a protein synthesis-dependent manner ( Gong et al., 2006; Ouyang et al., 1999). Tetanus-induced dendritic translation of CaMKIIα mRNA in CA1 pyramidal cells in acute hippocampal slices from WT and Paip2a−/− mice was examined. A surgical cut was made across the CA1 area perpendicularly to the pyramidal cell layer to separate tetanized and untetanized slice

regions ( Gong et al., 2006). Thirty minutes after tetanic stimulation, slices Thalidomide were fixed and processed for CaMKIIα fluorescent immunostaining, and the ratio of the CaMKIIα fluorescent signal from the dendritic area of the stimulated and the control sides was calculated. 1HFS induced no change in CaMKIIα amounts in WT slices ( Figures 7A and 7D), but in Paip2a−/− slices, 1HFS led to a significant increase in CaMKIIα expression (WT: 3.8% ± 1.9%; Paip2a−/−: 34.5% ± 9.7%, p < 0.01; Figures 7B and 7D). The increase in dendritic expression of CaMKIIα in Paip2a−/− slices was abolished when anisomycin was present during tetanization ( Figures 7C and 7D), demonstrating that increased levels of CaMKIIα protein is due to upregulation of CaMKIIα mRNA translation. These results indicate that, as with L-LTP, the threshold for induction of dendritic CaMKIIα mRNA translation is lowered in Paip2a−/− slices. It is striking that TBS increased CaMKIIα levels to a greater degree in Paip2a−/− slices than in WT slices (WT: 14.5% ± 2.3%; Paip2a−/−: 45.8% ± 15.4%, p < 0.05; Figure 7E), which supports in vivo results that demonstrate increased CaMKIIα mRNA translation following behavioral training.

We computed the probability of correct classification of trials in the preferred direction as fast or slow RT trials, based on firing rate in the eight cells with significant RT selectivity based on an ANOVA. Before coordinated movements to the preferred direction, coherent cells significantly

predicted whether a trial had a LY294002 fast or slow RRT (decode probability correct: 0.86; p < 0.001 binomial test) and a fast or slow SRT (decode probability correct: 0.72; p < 0.001). In contrast, not coherent cells did not significantly predict RRT (decode probability correct: 0.58, p = 0.16) or SRT (decode probability correct: 0.48; p = 0.56). Coherently active cells predicted RRT significantly better than cells that were not coherently active (p < AZD8055 order 0.005, two-sample binomial test). Coherently active cells also predicted SRT significantly better than not coherent cells (p < 0.05). Importantly, coherent cells encoded the speed of RTs only when movements were coordinated. When saccades were made alone, despite the fact that mean firing rate did not differ for reach and saccade versus saccade alone trials (Figures 5A and 5B), the decoder performed at chance (decode probability correct: 0.56,

p = 0.16). The not coherent cells also did not predict SRT (decode probability correct: 0.48, p = 0.56). The performance advantage of the coherent cell population in decoding RT was not due to the fact that there were more cells in the coherent population than the not coherent population. We repeated the analysis for increasing sizes of coherent and not coherent populations up to the number of available cells. The coherent population outperformed the not coherent population

for all cell subsets greater than two (Figure S2). Although we report here the results for eight cells, note that, for all numbers of coherent cells greater than three, the decoder performs best and above chance for RRT during coordinated movements. The decoder also performs well and usually above chance for SRT during coordinated movements at all numbers of cells but not for SRT during saccades made alone or for not coherent cells. We also examined whether the better decoding performance of the coherent cells could be due to their higher overall firing rate. When we subtracted the mean firing Suplatast tosilate rate from each cell before decoding the firing rate, we found that the results maintained the same pattern of significance. Coherently active cells predicted coordinated movement RT significantly better than cells that were not coherently active (RRT: p < 0.05. SRT: p < 0.01). Neither group of cells predicted SRT before saccades made alone (Coherent decode probability correct = 0.48. Not coherent decode probability correct = 0.46). Additionally, we decimated the firing rate of the significantly coherent units by 50% to match the firing rate of the not coherent units (see Experimental Procedures).