Interestingly, the distribution of Heine’s ‘archaeological’ bars does not match that of his radiocarbon dates: the centerpoints of two fall in the Colonial period, and one each in the Tlaxcala and Texcalac phases. On the basis of several dozen radiocarbon dates, I have documented the deposition of large volumes of alluvium between the Formative and Early Postclassic. In contrast, I have failed to positively identify any alluvium of Middle to Late Postclassic age. Downstream of Ladera, in an exposure of sandy near-channel

deposits with barely any sign of pedogenic development, a lens of charcoal buried at a depth of two meters yielded a date of 160 ± 40BP (Beta157074). This impinges on the end of the calibration data set, but the interval of highest probability at 1σ is AD1730-1780. The nature and stratigraphic context learn more of some other alluvia hint at CB-839 molecular weight a similarly recent date. At and east of La Laguna, many colluvial aprons grade into alluvial fan deposits. I have found several Postclassic and one apparently glazed sherd in them, but unfortunately in such low numbers and at shallow depths

that one cannot exclude intrusion from the modern ground surface. A cutbank of Los Ameyales is topped by more than a meter of bedded sands with no pedogenic imprint, likely derived from the erosion of the hillside of La Patada. Many barrancas (e.g., Concepción, Horcasitas, Coyotera) are bordered by ledges strewn with Middle to Late Postclassic sherds, sometimes on opposite banks of the same reach. Where the sherds are numerous, large and unabraded, excluding significant colluvial transport, this indicates that the stream has undergone an incision or major widening since the Postclassic. More precise dating of the onset new of incision, however, is often difficult, as exemplified by a cutbank at the foot of Loma La Coyotera. Its topmost palaeosol dates to 620 ± 50BP (Beta157070) and is buried by a wedge of colluvium. If the colluvium represents the activation of erosive processes in

the drainage that often precedes incision, the incision is more recent than the date. However, the span of the calibration (AD1280-1410 at 2σ), compounded by the uncertainty as to the residence time of the organic matter, and the delay in geomorphic response, mean that the stratigraphic sequence could be matched to any of rows A through E of Table 2. Sediment eroded off Las Margaritas now rests in a massive alluvial fan encroaching on and filling part of Lake Zacatepec. Postclassic sherds are present at the upper boundary of a soil buried on the lakeshore opposite the fan. This constitutes circumstantial evidence to link deposition to the abandonment of Las Margaritas, which I identify with Sacatepec, attested until at least the 1620s.

3). Combining the three catchments allows us to get a complete picture of the potential impact of anthropogenic disturbances in land cover for the Ecuadorian Andes. Three sites were selected for this study (Table 1). The Llavircay catchment (24 km2), the first site, is located in the Eastern Ecuadorian Cordillera. The two other study sites, the Virgen Yacu and Panza catchments (respectively 11 and 30 km2) are located within the Pangor catchment (283 km3) in the Western Cordillera

(Fig. 4). Topography is rather similar in the three sites. Elevation varies from 1438 m to 4427 m in Pangor and from 2017 m to 3736 m in Llavircay. Rivers are deeply incised and slope gradients are very steep (Fig. 4) with half of the slopes having Tariquidar in vivo slope gradients above 25° in Pangor and with one third VX-809 price of the Llavircay slopes above the mean angle of internal friction (estimated at 30° according to Basabe, 1998). The bedrock geology is composed of meta-volcanic and meta-sedimentary rocks; with andesite, rhyolite, limestone, conglomerate and chert in Pangor and phyllite, shale and quartzite in Llavircay. The Pangor catchment is exposed to the Pacific Ocean and influenced by El Niño. The climate can be described as equatorial mesothermic semi-humid to humid ( Pourrut, 1994). Mean annual precipitation is about 1400 mm but there is a high inter-annual

variability, with annual precipitation ranging between 475 mm (2002) and 3700 mm (1994) ( INAMHI, 2009). On the other hand, the Llavircay catchment is subjected to a warm and humid tropical climate ( Winckell selleck chemical et al., 1997) with mean annual precipitation of about 1330 mm and few inter-annual variability ( INAMHI, 2009). Detailed land cover maps of the three sites were constructed from aerial photographs, field surveys and a very high resolution image (for Pangor only). Aerial photographs at a 1:60,000 scale were available from the Instituto Geografico Militar for the years 1963, 1977 and 1989 (for Pangor) and 1963, 1973,

1983 and 1995 (for Llavircay). The very high resolution WorldviewII image was taken the 10th of September 2010 and has a spatial resolution of 2 m for multi-spectral bands and 0.5 m for panchromatic band. Field trips were realised in 2008, 2010 and 2011 to complete and validate the detailed land cover mapping. The land cover classification on aerial photographs was performed manually using a WILD stereoscope following Vanacker et al. (2000). The Worldview image was classified using visual interpretation of different false colour composite (band compositing) in ArcGIS. Spectral response patterns, texture analysis of the photographs (Lillesand and Keifer, 1994 and Gagnmon, 1974) and field validation allowed to distinguish eight land cover classes (Fig. 1, Fig. 2 and Fig.

Experimental and clinical studies increasingly show that alcohol-induced oxidative

stress is considered to be an early and indispensable step in the development of ALD [3]. Several pathways contribute to alcohol-induced oxidative stress. One of the central pathways is through the induction of cytochrome P450 2E1 (CYP2E1) by alcohol, leading to the induction of lipid peroxidation in hepatocytes [4]. Indeed, transgenic mice overexpressing CYP2E1 showed significantly increased liver damage following alcohol administration when compared with wild type mice [5]. By contrast, CYP2E1 knockout mice [6], and pharmacological inhibitors of CYP2E1 such as diallyl sulfide [7] and [8], phenethyl isothiocyanate [7] and [8], and chlormethiazole [9] decreased ethanol (EtOH)-induced lipid peroxidation and pathologic alterations. Chronic alcohol ingestion has been shown to increase levels of sterol regulatory element-binding protein-1 click here (SREBP-1), a master transcription factor that regulates lipogenic enzyme expression, including fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and stearoyl-CoA

desaturase-1 [10] and [11]. Alcohol intake also lowered levels of peroxisome proliferator-activated receptor-α (PPARα), a key transcriptional regulator of lipolytic enzymes, such as carnitinepalmitoyl-transferase-1 and uncoupling proteins [12]. In addition to regulating transcription factors associated with fat metabolism, alcohol affects the activities of enzymes involved in energy metabolism, including Vemurafenib purchase adenosine monophosphate-activated protein kinase (AMPK) and sirtuin 1 (Sirt1). AMPK, a conserved cellular energy status sensor, is a serine–threonine kinase that can phosphorylate and subsequently

inactivate SREBP-1 in hepatocytes, thereby attenuating steatosis [13]. Expression of the Sirt1, nicotinamide adenine dinucleotide-dependent class III histone deacetylase, is decreased in mice fed with alcohol, resulting in increased levels of SREBP-1 acetylation [14]. In addition, hepatocyte-specific knockout of Sirt1 impaired PPARα signaling and β-oxidation, Verteporfin mouse whereas overexpression of Sirt1 elevated the PPARα target gene expression [15]. Hence, the AMPK/Sirt1 signaling axis is a promising therapeutic target to attenuate lipogenesis and increase lipolysis in ALD. Korean ginseng (Panax ginseng Meyer) is one of the oldest and most commonly used botanicals in the history of traditional Oriental medicine. It has a variety of pharmacological activities, including anti-inflammatory, -tumor, and -aging [16]. The ginseng saponins, ginsenosides, play a key role in most physiological and pharmacological actions of ginseng [17]. Korean Red Ginseng (KRG) is heat- and steam-processed to enhance biological and pharmacological activities [18]. Red ginseng contains higher amounts of ginsenosides, and some ginsenosides are only found in red ginseng [19].

, 1984). Interestingly, in the present study, the control group presented a similar proportion of epithelial ciliated cells to what has been described in human beings without respiratory disease. In addition, OVA-induced airway allergic inflammation decreased the volume proportion

of epithelial ciliated cells and increased the volume proportion of goblet cells, a pattern that has been previously described in asthmatic patients (Knight and Holgate, 2003, Lumsden et al., 1984 and Spina, 1998). In the present study, we also observed that aerobic exercise (AE), in either non-sensitized or sensitized animals, increased the number of epithelial cells and decreased the number of ciliated cells in BAL fluid, phenomena previously elegantly demonstrated in non-sensitized animals Chimenti et al. www.selleckchem.com/products/bgj398-nvp-bgj398.html (2007). In this study, the authors also demonstrated that although AE increased the apoptosis of epithelial cells, the stimulus for epithelial proliferation was higher, resulting in a positive

balance or turnover of airway epithelial cells (Chimenti et al., 2007). Concerning the effects of AE on the airway epithelial cells of animals with allergic airway inflammation, we observed that although selleck kinase inhibitor AE decreased goblet cell hyperplasia, it did not modify mucus production (Fig. 1B). Although the functions of airway epithelium were initially described as protective, in the last few years, a variety of immunomodulatory effects have been attributed to these cells, i.e., the secretion of cytokines, chemokines, free radicals and growth factors (Bedard

and Krause, 2007, Boots et al., 2009, Bove et al., 2007, Broide et al., 2005, Dugger et al., 2009, Forteza et al., 2005, Pantano et al., 2008, Rennard et al., 2005 and van Wetering et al., 2007). In the present study, we demonstrate that AE in sensitized animals decreases OVA-induced epithelial expression of IL-4, IL-5, IL-13, CCL11, CCL5, adhesion molecules ICAM-1 and VCAM-1, iNOS and NF-kB. In addition, AE Protein kinase N1 increased the epithelial expression of anti-inflammatory cytokine IL-10 (Fig. 1). These results are extremely relevant, as AE reduces the epithelial expression of the main proteins involved in the inflammatory process in asthma, which are related to the eosinophilic and lymphocytic migration to the airways as well as to airway remodeling (Lilly et al., 1997, Puxeddu et al., 2006, van Wetering et al., 2007, Wilson et al., 2001 and Wong et al., 2006). In the present study, we also observed that AE reduced the epithelial expression of GP91phox and 3-nitrotyrosine and the peribronchial expression of 8-isoprostane (Fig. 3A). Increased levels of reactive oxygen (ROS) and nitrogen species (RNS) in asthma have been related with the release of pro-inflammatory and pro-fibrotic molecules through NF-kB activation (Bedard and Krause, 2007).

Thus, fosGFP expression is predictive of neurons with elevated firing activity in vivo. Because of the well-characterized delay between induction of fos expression and intrinsic GFP fluorescence, these data suggest that highly active neuronal subsets may be stable for hours in vivo.

To carry out a detailed mechanistic analysis of the cellular and synaptic basis of this increased firing within fosGFP+ neurons, we examined whether fosGFP expression was correlated with elevated spontaneous firing activity for layer 2/3 pyramidal neurons in acute brain slices, using paired-cell recordings. Spontaneous network activity at levels comparable to what was observed in vivo was facilitated by bathing slices in a low-divalent ACSF solution (Sanchez-Vives and McCormick, 2000, Maffei et al., AZD8055 solubility dmso 2004 and Shruti et al., 2008). Targeted cells were in midlayer 2/3 (232 ± 41 μm depth from pia, n = 26 cells; 45.5 ± 17 μm apart; n = 13 cell pairs). Because fosGFP expression is not induced by slice preparation (Barth et al., 2004), the stimulus responsible for induction of fosGFP expression was likely to have occurred at least several

www.selleckchem.com/products/gsk126.html hours prior to tissue preparation. Ex vivo, fosGFP+ cells maintained significantly higher rates of overall firing activity compared to neighboring fosGFP− cells (Figures 1G and 1H; firing rate for simultaneously recorded fosGFP− cells 0.050 ± 0.08 Hz versus fosGFP+ cells, 0.12 ± 0.14 Hz, n = 13, p = 0.01) . Elevated firing rates in fosGFP+ cells could be observed for until many hours (3+) after slice preparation and did not decline over the recording session. In wild-type animals, mean firing rates of individually recorded neurons were similar to those of fosGFP− neurons (Figure S1; 0.103 ± 0.023 Hz, n = 30, p = 0.9). However, a subset of wild-type neurons exhibited high firing rates comparable to those observed in fosGFP+ cells, suggesting that this subset is present in wild-type animals but can be uniquely visualized in fosGFP transgenic mice. In both our experiments and others’ (Steriade et al., 1993, Sanchez-Vives and McCormick, 2000 and MacLean et al., 2005), spontaneous firing in neocortical

neurons ex vivo tends to occur during epochs of depolarization, similar to what has been termed Upstates in vivo. Although the precise trigger for these events is unknown, epochs are observed in both neurons that fire frequently and those that do not fire at all, where they appear as prolonged subthreshold events (Figure 2). Are fosGFP+ neurons differentially recruited during these epochs of network activity? FosGFP+ cells fired more spikes during a depolarizing epoch compared to fosGFP− cells, although epoch duration was identical (fosGFP− 2.7 ± 0.17 s, n = 134 epochs over 18 cells, versus fosGFP+ 2.7 ± 0.14 s, n = 149 epochs over 18 cells, p = 0.8). FosGFP+ cells showed significantly more spikes per epoch (s/e) than simultaneously recorded, neighboring fosGFP− cells (Figure 2C; fosGFP− 3.61 ± 0.

Whether or not similar mechanisms control cortical regionalization in humans has been ERK inhibitor difficult to establish, because manipulating transcription factor expression in highly controlled genetic backgrounds is not feasible. In this issue of Neuron, Chen and colleagues ( Chen et al., 2011) take on this challenge by using a potent combination of analytical strategies, a twin-study design and structural MRI, to address whether latent genetic factors contribute to regionalization of the cerebral cortex in humans. Specifically, by obtaining and analyzing MRI data from over 200 monozygotic and dizygotic twin pairs (from

the Vietnam Era Twin Study of Aging) ( Kremen et al., 2006), the authors derived cortical surface reconstructions using a spherical atlas mapping procedure to measure the relative contributions of genetic and environmental influences on the regional expansion of cortical surface area. In this way, they could generate a map that reveals a regional pattern of shared genetic influence on cortical surface area. Interestingly, they demonstrate that along the anterior-posterior axis, there is evidence for both positive and negative

genetic correlation effects on surface area. When related to a seed region in the frontal Tyrosine Kinase Inhibitor Library pole, positive correlations are seen to be strongest nearest the seed and to then taper off posteriorly to the central sulcus, where there is an abrupt transition to negative correlations that are still more posterior. The “push-me/pull-you” Bcl-w nature of these

relationships is highly reminiscent of the antagonistic relationship seen along the cortical anterior-posterior axis between transcription factors PAX6 and EMX2 in mouse studies (O’Leary et al., 2007). The authors also nicely demonstrate that the locations of transitions in shared genetic influence were comparable when derived via a seed-based approach or via a data-driven approach. These findings convincingly illustrate a pattern of genetic correlation for cortical surface area that reflects the aggregate effect of myriad genetic/intrinsic mechanisms. However, these results should not be construed as a cytoarchitectonic map of neocortical arealization or as a map that reveals the expression pattern of putative human homologs of the transcription factors described in the mouse literature. First, the granularity of the regionalization is at a scale larger than one would consider to be associated with neocortical areas. Rather, the regionalization appears to be of a lobar (such as frontal or parietal) or sublobar, not areal, scale. For example, the data reveal no evidence of a delineation between V1 (primary visual cortex) and V2 on the medial surface.

Postembedding immunogold localization of GABA was used to identify inhibitory synapses onto somata in L2/3 of V1. The area of GABA-positive axon terminals and proportion of mitochondria per terminal were not different between WT and Ube3am−/p+ mice Selleckchem BKM120 ( Figures 4A2 and 4A3). However, there was a decrease in the number of synaptic vesicles, and a large increase

in the number of clathrin-coated vesicles (CCVs), in the Ube3am−/p+ mice compared to WT ( Figures 4A4 and 4A5 and S4F and S4G). We also tested whether the defects we observed in inhibitory synapses were generalized to excitatory synapses. Similar to inhibitory synapses, we observed a decrease in the number of synaptic vesicles, but no change in the area of excitatory axon terminals or the proportion of mitochondria per terminal ( Figures 4B1–4B4 and S4D and S4E). Finally, we saw little or no decrease in the number of CCVs at excitatory synapses between genotypes ( Figures 4B5 and S4D and S4E). These data suggest a defect in synaptic vesicle cycling in inhibitory synapses of Ube3am−/p+ mice. Previous studies examining synaptic vesicle cycling have identified genes whose mutation leads to increased numbers of CCVs in axon terminals (Slepnev and De Camilli, 2000). Many of these mutant synapses maintain the ability to release neurotransmitter and have normal short-term plasticity; however, during

periods of high activity these synapses fail to adequately replenish their synaptic vesicle pool, resulting in a delayed recovery Pravadoline to baseline levels of transmitter high throughput screening compounds release (Luthi et al., 2001). These studies led us to

test whether inhibitory synapses in the Ube3am−/p+ mice had functional deficits similar to other synaptic vesicle cycling mutants. We applied a train of 800 stimuli at 10 Hz while recording eIPSCs in L2/3 pyramidal neurons in WT and Ube3am−/p+ mice ( Figure 4C). We then decreased the stimulation frequency to 0.33 Hz and recorded the recovery phase of the eIPSC ( Figure 4C1). Ube3a loss had no effect on the depletion phase of the eIPSC ( Figure 2C2) in agreement with our previous experiments examining short-term plasticity ( Figures 1I and 3B). However, we found a large decrease in the rate and level of recovery of the eIPSC in Ube3am−/p+ mice compared to WT ( Figure 4C3). These data are consistent with defects in inhibitory synaptic vesicle cycling in Ube3am−/p+ mice. Specifically, the decrease in recovery of the eIPSC, combined with the increase in CCVs, suggests an inability of newly endocytosed CCVs to reenter and replenish the synaptic vesicle pool. These defects may render a subset of inhibitory synapses nonfunctional in Ube3am−/p+ mice. Finally, we challenged excitatory synapses with the same high frequency stimulation protocol that we used to test inhibitory synapses (Figure 4D1). Unlike inhibitory synapses, Ube3a loss did not have an effect on the recovery of excitatory synapses from high-frequency stimulation (Figure 4D3).

This difference of 5–10 days is probably critical because heterotopic grafts of rat E12 cortex target subcortical regions defined by the recipient graft site, whereas the targets of rat E14 grafts are defined by the cortical area from which the donor cells originated (Gaillard et al., 2003 and Pinaudeau et al., 2000). Whether the respecification occurred at the level of progenitor cells or the neurons produced by them was not determined, but it seems likely that rat E12 neural progenitor cells are still capable of responding to the morphogen click here gradients present within in the developing cortex by adjusting their transcription factor

levels, whereas the areal identity of rat E14 progenitor cells is fixed. E12 and E14 in the rat are equivalent to ∼E10.5 and ∼E12.5 in the mouse (Schneider and Norton, 1979), and mouse subcortical projection neurons are not produced until after E12.5 (Polleux et al., 1997 and Takahashi et al., 1999). Thus, the areal identity of mouse cortical progenitor cells is probably fixed by E12.5, and the transplanted cells of Ideguchi et al. (2010) presumably Pictilisib had not yet reached this stage. More detailed analyses will be needed to

precisely determine the stage of neural differentiation at which targeting potential becomes fixed and to learn the molecular changes responsible for this loss of plasticity. The plasticity of early cortical neuroepithelial cells may present an opportunity to circumvent the requirement for areal specification in vitro if cells are transplanted after dorsal telencephalic fate is fixed, but while areal identity is still plastic. However, this strategy would entail losing the ability to transplant a single neuronal subtype given that early cortical progenitors will likely proceed through the known temporal sequence of neuronal subtype production—a drawback in some situations. There may also be less control over the final dose of transplanted cells because Montelukast Sodium proliferation will occur after transplantation. Finally, the less

differentiated and more proliferative the cells are at the time of transplantation, the greater the risk of neural overgrowth (Elkabetz et al., 2008), so the stage of neural differentiation and the expected amount of proliferation would have to be very precisely controlled and accounted for. Although progress is being made on elucidating the transcriptional regulation of fate specification of cortical excitatory neurons (Table 2) (Arlotta et al., 2005, Leone et al., 2008 and Molyneaux et al., 2009), little is known about the molecular mechanisms that govern which subtype of cortical neuron is produced by a radial glial (RG) cell division at different times during neurogenesis (Figure 1D). Here, we will focus on the feasibility of producing a single subtype of neuron from progenitor cells that are programmed to produce several cell types in a defined sequence.

The DOR activation-induced reduction of the number of MORs on the cell surface could be important in the regulation of the neuronal sensitivity to μ-opioids. The MOR/DOR interaction may be enhanced by opioid agonist stimulation and Selleckchem Docetaxel membrane depolarization that induce the surface expression of intracellular DORs in the pain pathway (Bao et al., 2003, Cahill et al., 2001, Ma et al., 2006, Patwardhan et al., 2005 and Walwyn et al., 2005). Prolonged morphine treatments increase the

cell surface expression of intracellular DORs (Gendron et al., 2006 and Morinville et al., 2003) and the MOR/DOR heteromerization in DRG neurons (Gupta et al., 2010). Although our immunostaining procedure may not be sensitive enough to detect low levels of DORs in the dorsal horn neurons, prolonged morphine treatments also induce a surface expression of see more DORs in spinal interneurons (Morinville et al., 2003). Therefore, chronic morphine treatments may enhance the DOR-mediated inhibitory effects

on the MOR activity. It is also possible that surface-expressed DORs are accessible to opioid peptides, such as ENK, that are released from spinal interneurons (Cesselin et al., 1989) and would thus be involved in the regulation of MOR activity in afferent terminals. It is noteworthy that the TAT peptide can serve as a guiding signal in the MORTM1-TAT protein, enabling the insertion of the exogenous TM1 peptide into the plasma membrane

in the direction that is required for its function. This method provides an approach to analyze the functional roles of a receptor interaction in vivo by physically dissociating two types of GPCR in the plasma membrane, while maintaining the function of each type of GPCR. The identification of the heteromerization interface of GPCRs is required for designing a molecular probe that effectively disrupts the receptor interaction. The present study shows that the insertion direction of the transmembrane domain of a receptor can be determined by the fusion of the TAT peptide at either the C or N terminus. Dextrose This determination is based on both the identification of the transmembrane domain specifically mediating the receptor interaction and the membrane penetration capacity of the TAT peptide. Using such an approach to specifically disrupt the physical interaction between receptors and/or ion channels in the plasma membrane is not only a tool for the functional analysis of the membrane protein interaction in vivo but also a potential strategy for medical intervention. The present study shows that a systemically applied MORTM1-TAT protein disrupts the MOR/DOR interaction in the spinal cord and improves morphine analgesia. This result is consistent with findings on enhanced morphine analgesia obtained by other pharmacological or genetic approaches.

Such a precession would result in fully inconsistent gamma phase relations and a complete absence of gamma coherence. Gamma coherence would actually be destroyed by any of the observed frequency differences: a 6 Hz frequency difference would lead to complete precession and loss of coherence six times per second, and a 2 Hz difference would lead to complete precession and loss of coherence two times per second. PI3 kinase pathway An absence of coherence would be inconsistent with CTC. However, we found clear V1-V4 gamma coherence. The presence of gamma coherence demonstrates that gamma phases did not freely precess against each other, but rather that gamma rhythms had a consistent phase relation. Thereby, the

observation of coherence rules out the abovementioned simple interpretation of the slight frequency differences. Rather, the synopsis of our findings suggests one of the following scenarios or a combination of them: (1) the frequencies of the synchronized rhythms at the V4 site and the relevant V1 site are always identical on a moment-by-moment basis, yet the common frequency fluctuates and the local circuits resonate at different frequencies, giving rise to different peak frequencies in the time-averaged power spectra; (2) our ECoG recordings in V4 reflect a mixture of (at least) two gamma rhythms in V4, one entrained by the attended V1 gamma and a second at a slightly lower

frequency; and (3) in the third scenario, the different gamma frequencies play mechanistic roles in bringing about the selective interareal synchronization. There is one crucial additional ingredient to this scenario, namely a theta-rhythmic gamma-phase reset across mTOR inhibitor V1 and V4, which we have described previously

(Bosman et al., 2009). After the reset, the attended V1 gamma and the unattended V1 gamma partly precess relative to the slightly slower V4 gamma. The attended V1 gamma is of higher frequency than the unattended V1 gamma and therefore precesses faster. Correspondingly, in each gamma cycle, the attended V1 input enters V4 before the unattended V1 input. The earlier entry together with feedforward inhibition makes the attended V1 input entrain V4 at the expense of the SB-3CT unattended V1 input (Fries et al., 2007; Vinck et al., 2010). The selective entrainment of V4 by the attended V1 gamma rhythm further enhances the gain of the attended V1 input and reduces the gain of the unattended V1 input (Fries, 2005; Börgers and Kopell, 2008). The theta-rhythmic reset of interareal gamma-band synchronization is supported by our data (Figures 8 and S4). It probably corresponds to a reset of attentional selection and, under natural viewing conditions, might subserve the theta-rhythmic sampling of multiple objects in a scene, either overtly (Otero-Millan et al., 2008) or covertly (Fries, 2009; Landau and Fries, 2012). Importantly, the third scenario, with partial precession, also leads to selective coherence, as observed here.