, 2008) This competition can be biased by many factors, such as

, 2008). This competition can be biased by many factors, such as expected gain (Platt and Glimcher, 1999), subjective strategies (Dorris and Glimcher, 2004), or indeed any factor relevant to the choice. Dorris and Glimcher (2004) proposed the term “relative subjective desirability” to imply that Panobinostat chemical structure what modulates neural activity during decision tasks is a subjective variable that depends upon the relative desirability of one option versus another. Klaes et al. show that the modulation of neural activity is indeed related to subjective desirability. A recent study in

our lab (Pastor-Bernier and Cisek, 2011) shows that this neural modulation is related to relative, rather than absolute, desirability. In our study, monkeys made decisions between two targets whose stimulus features indicated how many drops of Selleckchem SP600125 juice each was worth, and we examined whether neural activity in PMd reflected a competition between the two potential reaching actions. As expected, we found that neural activity increased as the value of the preferred target increased while the other target’s value was constant. We also found that if we kept the preferred target’s value constant

and increased the other target’s value, neural activity decreased, suggesting a competitive interaction. Most importantly, if only a single target was presented then neural activity was completely insensitive to its value—strongly suggesting that in all cases, activity specifying potential actions is modulated by the subjective desirability

of those actions relative to other options. This further strengthens the proposal made by Klaes et al. that the modulation of activity in PMd and PRR reflects subjective preferences for one action goal over another. The question of how the brain makes decisions is the ADAMTS5 topic of many recent and ongoing studies. Klaes et al. provide a critical piece of the puzzle by showing that the brain is capable of simultaneously applying two rules to the same sensory information in order to specify two parallel potential action goals in the sensorimotor regions of frontal and parietal cortex. They show that these activities do not simply reflect sensory information, nor do they simply reflect the motor options, but that they reveal the animals’ strategies and subjective preferences. Taken together with other studies cited here and in Klaes et al., these findings support an “intentional” framework for sensorimotor behavior (Shadlen et al., 2008), whereby the brain makes decisions about actions through a biased competition taking place within the same system that guides the execution of those actions (Cisek, 2006). Although the brain can also make purely perceptual decisions in situations where no response has yet been specified (e.g., Bennur and Gold, 2011), the strategy of specifying multiple potential actions appears to be adopted in all situations in which it is possible.

We then delivered a train of ten stimuli at 100 Hz to the TA path

We then delivered a train of ten stimuli at 100 Hz to the TA pathway followed by a single SC stimulus 20, 40, 60, or 80 ms after initiating the TA train. We found that in this paradigm, SC and SLM stimuli that were subthreshold when delivered alone were able to produce a spike when paired ( Figure 7D), indicating that this spike-enhancing

phenomenon originally observed in adult rats ( Remondes and Schuman, 2002) also occurs in developing mice. During the dual stimulation protocol, we interleaved sweeps during which we only stimulated one pathway to ensure that the single stimuli remained subthreshold throughout the duration of the experiment. We quantified normalized spike probability by dividing the number of sweeps in which the cell fired an action potential by the total number of dual stimulation sweeps and then dividing this value phosphatase inhibitor library by the amplitude of the FV recorded in SR. This value represents the spike probability for a given number of stimulated axons. We found that the normalized spike probability was significantly reduced in NGL-2 CB-839 clinical trial KO animals when the SLM-SR interval was 40, 60, and 80 ms, and there was a similar trend when the interval was 20 ms ( Figure 7E). We quantified a normalized value for SR-evoked EPSP by dividing the recorded EPSP amplitude by the amplitude of the SR fiber volley. We found that this value was significantly reduced

in NGL-2 KO mice ( Figure S4A). There was no difference Dipeptidyl peptidase in peak amplitude of the TA-evoked EPSP, resting membrane potential, or input resistance between conditions ( Figures S4B–S4D). Together, these data demonstrate that reduced SR synapse density resulting from loss of NGL-2 impairs cooperative interactions between SC and TA synapses in CA1 cells. Thus, the level of NGL-2 expression strongly influences the integrated output

of CA1 neurons. In the CNS, a postsynaptic neuron typically receives synaptic input from a variety of distinct sources, but the molecular mechanisms that give rise to the formation of these different classes of synapses are not well understood. Our study demonstrates that the postsynaptic adhesion molecule NGL-2 plays a critical role in regulating the Schaffer collateral synapses onto CA1 neurons without affecting other excitatory inputs. The synapse specificity of NGL-2 action appears to be mediated by selective localization of the protein to the domain of the apical dendrite where CA1 neurons receive Schaffer collateral inputs (Figure 8). NGL-2 belongs to an LRR protein subfamily that includes NGL-1 and NGL-3, which are all expressed widely throughout the CNS (Kim et al., 2006) but interact with different presynaptic receptors (Kim et al., 2006; Lin et al., 2003; Woo et al., 2009b) that are expressed in discrete neuronal populations (Kwon et al., 2010; Nakashiba et al., 2002; Yin et al., 2002).

Subjects were excluded if they had an Axis I diagnosis, active or

Subjects were excluded if they had an Axis I diagnosis, active or recent substance abuse, or if they had a first-degree relative with a known or suspected Axis I disorder based on family history questionnaire. Controls were 52.2% female, had a mean age of 48.4 ± 18.6 years and an estimated IQ of 105.0 ± 12.4. All subjects were Caucasian by self-report and drawn from a single geographic location (Glen Oaks, NY area). Although population stratification is a potential confound in any case-control study, we have previously demonstrated that undetected substructure is not present in our

geographically homogeneous population. In a genome-wide association buy KU-55933 study of a case-control cohort collected by the same methods described above ( Lencz et al., 2007), we tested for stratification using 210 ancestry informative markers selected for maximal informativeness and observed no differences between patients and controls beyond chance levels. Moreover, none of the subjects in the cohort deviated from a single population as assessed by the STRUCTURE program ( Pritchard et al., 2000). Patient diagnosis was

established through structured interview (Structured Clinical Interview-DSM-IV; SCID-IV) ( First et al., 1998) and confirmed by diagnostic consensus conference, which utilizes expert clinical opinion alongside SCID-IV data and corroborating medical record information. Healthy controls for the project were assessed using the Structured Clinical Interview for DSM-IV, MLN8237 nmr Non-Patient

edition, specifically designed for healthy subjects to rule out Axis I diagnoses. In addition to the structured diagnostic interview, potential subjects were screened to rule out any history of CNS trauma, neurological disorder, or diagnosed learning disability. FEZ1 genotyping procedures were carried out using the Affymatrix 500K platform as previously described ( Lencz et al., 2007). Briefly, genomic DNA was extracted from whole blood and hybridized to two chips containing ∼262,000 and ∼238,000 SNPs based on manufacturer’s specifications. Patients and controls were proportionally Oxalosuccinic acid distributed on each 96-well plate. Genotype calls were made using Bayesian Robust Linear Model with Mahalanobis distance classifier algorithm threshold at 0.5 applied to batches of 100 samples. Mean call rates <90% on both chips, or <85% on one chip, were rejected, resulting in a mean call rate for the retained sample of 97%. Allele frequencies, Hardy-Weinberg equilibrium (HWE), and linkage disequilibrium structure were examined using Haploview 3.32 ( Barrett et al., 2005). The four SNPs formed a single haplotype block as shown in Figure 6A. For FEZ1 association with illness, none of the four SNPs in the haplotype deviated from HWE (p > 0.05). χ2 test statistics were used to test for allelic and genotypic associations to schizophrenia for single SNPs, as well as for group differences on haplotype frequencies.

E brunetti was never identified using the multiplex PCR in one-

E. brunetti was never identified using the multiplex PCR in one- or two-tube formats. Accurate identification of Eimeria

spp. is important not only for the diagnosis of disease but also for management of subclinical infection, development and application of effective control strategies, and biological and epidemiological study ( Lee et al., 2010 and Sun et al., 2009). Traditionally, identification of Eimeria spp. has been based on the morphological characteristics of oocysts, parasite biology, Lapatinib datasheet clinical signs of the affected animals, and the typical macroscopic lesions assessed during necropsy ( Long and Joyner, 1984). However, in a natural setting mixed infections of different Eimeria spp. are commonly encountered and morphological characteristics and pathological changes may overlap, hindering accurate diagnosis and undermining detection of subclinical disease ( Long and Joyner, 1984 and Rice and Reid, 1973). Thus, it has been suggested that these methods should not be used in isolation selleck for differentiation of Eimeria

species ( Long and Joyner, 1984 and Lopez et al., 2007). Alternatives include molecular or computational approaches such as PCR, qPCR and the software COCCIMORPH. PCR assays capable of identifying and differentiating Eimeria spp. have been available for more than 20 years but, despite recognition as the ‘gold standard’ of detection for many pathogens, this technology is yet to replace traditional coccidial diagnostics ( Brook et al., 2008, Olano and Walker, 2011 and Stucki et al., 1993). Features of eimerian biology including the resistance of the oocyst wall to anything other than mechanical disruption, limiting access to template DNA (for most avian-infecting species), and PCR inhibition by the surrounding faecal material have discouraged use of PCR. While several PCR assays have been

described to identify specific Eimeria species very few studies have focused on the applicability of these techniques for identifying Eimeria spp. in commercially raised poultry throughout the world ( Carvalho et al., 2011a, Carvalho et al., 2011b, Frölich et al., 2013 and Haug et al., 2008). Development of a standardised protocol supporting medium throughput Endonuclease diagnostic sampling for Eimeria will enhance the value of such data while promoting the application of PCR and comparison between studies. Following collection of fresh environmental faecal samples we explored two DNA extraction procedures and the influence of residual faecal contamination. The inclusion of faecal material dramatically reduced PCR sensitivity with genomic DNA purified using the QIAamp DNA Stool kit, supporting the value of even a rudimentary pre-extraction parasite purification step. The cause of this inhibition remains unclear at present. The InhibitEx step of the Stool kit protocol is designed to adsorb substances that can degrade DNA and inhibit downstream enzymatic reactions and should minimise PCR inhibition.

We compared

the maturation index of pairs of synapses wit

We compared

the maturation index of pairs of synapses within the same MSB contacting mHRP-positive imaged dendrites and mHRP-negative dendrites whose dynamic history is unknown. For boutons that contact stable mHRP-labeled dendrites, the maturation indices of the synapses contacting both the mHRP-labeled and unlabeled are relatively correlated (R2 = 0.64; Figure 4F). The boutons this website that contact dynamic mHRP-labeled dendrites form synapses with more heterogeneous maturation indices, which are less correlated (R2 = 0.25; Figure 4F). This analysis indicates the afferents establish divergent contacts with multiple postsynaptic neurons within a limited space by using MSB structures and that divergence from individual boutons to multiple postsynaptic partners decreases as individual MSBs lose some synaptic contacts, while others remain and become mature. Retinotectal synaptogenesis visualized by in vivo two-photon time-lapse imaging of fluorescent protein-tagged

synaptic vesicle proteins indicates that presynaptic sites assemble over a time course of hours (Alsina et al., 2001, Meyer and Smith, 2006 and Ruthazer et al., 2006). To examine the configuration of nascent click here synapses formed on recently extending dendrites, we collected images of tectal neurons at 0 hr, 4 hr, and 8 hr, a protocol we previously demonstrated captures branch dynamics (Sin et al., 2002). We created a partial 3D EM reconstruction of a dendritic arbor imaged with this rapid protocol and mapped the locations of synapses on stable and extending dendrites (Figures 5A–5M). Synapse density on dendrites extended within the previous 4 hr (0.67 ± 0.12 synapses/μm for 42.6 μm in 6 branches) was significantly higher than on branches that were stable over the 4h imaging period (0.42 ± 0.07 synapses/μm for 73.9 μm in 5 branches, p < 0.05; Figure 5N). In addition, we often observed that axonal boutons

contacting extending dendrites, which had at most crotamiton a 4 hr lifetime, contained dense core vesicles (Figure 5M), consistent with the idea that they are involved in synaptogenesis (Li and Cline, 2010). As observed in the neuron imaged at daily intervals (Figure 2A), extending dendrites formed synapses with MSBs. Axon boutons contacting extending dendrites had more postsynaptic partners than boutons contacting stable dendrites (extended: 1.95 ± 0.18, n = 23; stable: 1.35 ± 0.09, n = 29; p < 0.05; Figure 5O). Furthermore, when we determined the average maturation index of synapses in each MSB, we found that MSBs contacting extending branches had lower average maturation indices than MSBs contacting stable dendrites (17.8 ± 2.4 versus 41.1 ± 2.2, n = 23 and 29, p < 0.05; Figure 5P). As described above, the MSBs contacting the mHRP-labeled dendrites from the imaged neuron also contact neighboring unlabeled dendrites.

We observed a significant decrease of current amplitudes at highe

We observed a significant decrease of current amplitudes at higher concentrations of α5, and this effect was significantly more pronounced with α5 D397N. These results suggest that α5 and β4 may compete for binding to α3, in line with the studies showing such competition for binding to α4 ( Gahring and Rogers, 2010). Given that overexpression of β2 with either α3 (Figure 1A) or α4 (Figure S1B) did not increase currents,

we were interested in identifying the residues differing between β4 and β2 that mediate this effect. Since the long cytoplasmic loop is the most divergent domain between nAChR subunits (Figure S1C), and since it has been implicated in cell-surface expression and trafficking of β2 subunits (Nashmi et al., 2003 and Ren et al., 2005), we generated β2–β4 chimeras exchanging either this domain, or short motifs Protein Tyrosine Kinase inhibitor and single residues within this domain. Replacement of the cytoplasmic loop of β2 with the corresponding sequences present in β4 (β2/β4 322–496) led to strong increase of nicotinic currents (Figure 1C). Introduction of two β4-specific motifs (a serine/tyrosine rich motif [β2/+β4 382–391] and gephyrin-like-binding motif [β2/+β4 401–419] into the β2 loop) had no influence on current amplitudes (Figure 1C). We next performed bioinformatic analyses and 3-Methyladenine nmr singled out eight β4-specific residues (indicated as T-1 to T-8 in Figure S1C) present

within highly conserved motifs. Six of these residues were not

further considered: T-2, T-3, T-6, and T-7 residues differ between mouse and chicken β4 subunits, which are equally potent in enhancing nicotine-evoked currents (Figure S1B); T-4 residue lies within the tested motif in the β2/+β4 382–391 chimera; and residues at position T-8 have the same charge (Figure S1C). The remaining two candidates, T-1 (S324 in β4 and T327 in β2) and T-7 (S435 in β4 and R431 in β2) (Figure S1C) were tested by point mutagenesis in the β2 subunit backbone. The β2 T327S point mutant did not increase current, whereas replacement of β2 R431 with serine resulted in a 3.5-fold current increase (Figure 1C). Furthermore, ever point mutation of the native S435 in the β4 subunit to the arginine residue present in β2 (β4 S435R) abolished the β4-specific activity. Thus, these data demonstrate that the distinctive ability of β4 to increase currents when overexpressed maps to a single residue (S435) that is required in β4 for current increase and can confer this property to β2. Alignment of mouse, human, and Torpedo nAChR subunit sequences indicated that S435 in β4 and D397N in α5 are located in the 25 amino-acid-long amphipathic membrane-associated stretch (MA-stretch) described in the Torpedo subunits ( Unwin, 2005) ( Figure 2A). Electron microscopy studies of the Torpedo nAChR have proposed a 3D density map of the receptor complex.

B ), a Columbia University Undergraduate WEP grant (S K C ), a 5U

B.), a Columbia University Undergraduate WEP grant (S.K.C.), a 5U01 MH078844-05 grant (Z.J.H.), and the Howard Hughes Medical Institute (S.A.S.). “
“In February 1637 in Amsterdam, the cost of a single exotic tulip bulb reached a price equal to ten times what a skilled craftsman earned in a year. The price of the same bulb collapsed a few days later. The dramatic rise and fall of tulip bulb prices is a famous historical example of a financial bubble (Kindleberger and Aliber, 2005). A bubble is conventionally defined by active trading of an asset at prices that are considerably higher than its intrinsic fundamental value. Examples of modern bubbles

include Japanese stocks in the 1990s, the US high-tech sector in the late 1990s, and housing prices, which rose and crashed in many countries from 2000–2008. All of these bubbles Akt cancer (especially the housing crash) caused long-lasting macroeconomic disruptions (Shiller, 2005). Modern bubble episodes have also led to a substantial shift in thinking about the capacity of prices to act as sober information aggregation mechanisms that guide efficient allocation of capital. Policy makers, academics, and market participants alike are now more familiar with, and groping to understand, the ways that prices can reflect pathological valuation and are actively debating Ku 0059436 whether policy

interventions can help (Akerlof and Shiller, 2009). Despite these dramatic historical and modern examples, there is no well-accepted theory of how bubbles start and end. One common definition of bubbles is rapid price appreciation followed by a crash (Brunnermeier, 2008). However,

this definition has no predictive power for identifying an ongoing bubble, since it does not identify a bubble before it crashes. Furthermore, fundamental asset values are rarely known with precision, so it is difficult to identify a bubble if bubbles are defined as prices above an elusive fundamental value. One way to learn about bubbles is to observe trading in an experimental market for artificial assets that have a known fundamental value. In these markets, price variation cannot be explained by changes TCL in fundamentals. In fact, several carefully controlled economics experiments have shown that certain classes of asset markets do generate price bubbles quite regularly, even when intrinsic values are easy to compute and are known to traders (Smith et al., 1988, Camerer and Weigelt, 1993, Porter and Smith, 2003 and Lei et al., 2004). The nature of bubbles has also been intensely investigated in theory (Abreu and Brunnermeier, 2003 and Yu and Xiong, 2011), but empirical reasons why bubbles arise and then crash are still not well understood in economics (Xiong, 2013). Recent work in neuroeconomics has shown how financial decision theory can be informed by neuroscientific data (Bossaerts, 2009). In particular, studies have started to dissect the neural mechanisms by which risk processing (Preuschoff et al.

3 kHz from the output

3 kHz from the output JQ1 of the Multiclamp 700B amplifier. Calculations used look-up tables for the voltage dependence of τ(Vm) and n∞(Vm) and were completed in 40 μs. I(t) was then updated with 8 pA resolution, low-pass filtered at 10 kHz and injected into the cell via the Multiclamp 700B amplifier. Improper bridge balance (e.g., >20 MΩ or changed by  >∼2MΩ) caused strong oscillations that in some cases even triggered spikes. Only recordings without such oscillations were analyzed. Outside-out patches were pulled from identified OFF Alpha ganglion

cells in order to study voltage-gated currents. After establishing a seal of >5 GΩ on the soma and correcting for the pipette capacitance, the cell membrane was disrupted to establish a whole-cell configuration with Vhold = −60mV. The pipette was slowly removed from the cell using the manipulator’s piezo drives, while

constantly checking Rs, Rin, and capacitance. After reaching >100 MΩ of Rs (from originally 10–20 MΩ), the pipette was quickly pulled away from the cell by several hundred micrometers. Initial membrane capacitance and Rin were recorded from the membrane patch. Cases where Vm was positive VE-822 mw to −30 mV or when the ratio of Rin to Rs was <10 were not studied further. Voltage-clamp recordings were performed without Rs compensation at 10 kHz with a 4 kHz Bessel filter. Capacitance artifacts and leak currents were measured during the voltage-clamp recordings with 5 mV steps from Vholds and used to record changes in membrane parameters. Recordings with roughly constant leak current were used for analysis. Capacitance artifacts were fitted with Thymidine kinase a double exponential

function and together with the leak current subtracted from the current traces. Because of imperfect fits of the first two recorded points in the capacitance artifact, the first 0.2 ms after a voltage step were omitted. We thank Mania Kupershtok for technical assistance and Dr. Josh Singer for comments on the manuscript. Supported by a Research to Prevent Blindness Career Development award, an Alfred P. Sloan Foundation fellowship and the National Institutes of Health (EY14454; EY14454-S1; core grant EY07003). “
“The activity of even a single thalamic axon can generate robust, widespread inhibition in somatosensory cortex (Swadlow and Gusev, 2000 and Swadlow and Gusev, 2002). This is not because thalamic afferents are inhibitory—they release the excitatory transmitter glutamate (Kharazia and Weinberg, 1994)—but because they can efficiently fire cortical inhibitory neurons through one of the cortex’s most powerful synapses (Cruikshank et al., 2007, Gabernet et al., 2005, Hull et al., 2009, Porter et al., 2001, Swadlow and Gusev, 2000 and Swadlow and Gusev, 2002). These GABAergic interneurons in turn synapse onto local excitatory neurons, creating a robust feedforward inhibitory circuit (Gabernet et al., 2005, Inoue and Imoto, 2006 and Sun et al.

, 2010) To test whether PrP and α2δ-1 interacted physically, we

, 2010). To test whether PrP and α2δ-1 interacted physically, we immunoprecipitated PrP from cerebellar extracts of Tg(WT) and Tg(PG14) mice, and immunoblotted the precipitated fractions with an antibody raised against the α2 polypeptide of α2δ-1. As shown in Figure 5A, an immunoreactive band of ∼145 kDa was detected in immunoprecipitates of Tg(WT) and Tg(PG14)

but not in Prnp0/0 mice, or when the immunoprecipitation was done in the absence of the anti-PrP antibody. After deglycosylation with PNGaseF, this band shifted to an apparent molecular Raf inhibitor weight of 107 kDa, as expected for the α2 polypeptide ( Figure S5A) ( Davies et al., 2006). The interaction was confirmed in the reverse experiment in which α2δ-1 was immunoprecipitated Anti-diabetic Compound Library from cerebellar extracts and PrP detected by immunoblot (Figure 5B), and was also seen in primary cultured CGNs (Figure S5B) and transiently transfected HeLa cells (Figure S5C). HC-deleted PrP molecules coimmunoprecipitated with

α2δ-1 (Figure S5C), indicating that PrP region 114–121 was not essential for the interaction. Next, we tested whether the distribution of α2δ-1 was altered in cells expressing PG14 PrP. HeLa cells were cotransfected with plasmids encoding the CaVα1A, CaVβ4, and α2δ-1 subunits, and either wild-type or PG14 PrP-EGFP fusion proteins, and analyzed by confocal microscopy after immunofluorescent staining of α2δ-1. Consistent with previous localization of nonfluorescent and EGFP-fused PrPs (Biasini et al., 2010, Fioriti et al., Farnesyltransferase 2005 and Ivanova et al., 2001), the majority of wild-type PrP localized on the cell surface (Figures 6A and 6J), whereas PG14 PrP was mostly found in intracellular

compartments (Figures 6D and 6J). In cells expressing wild-type PrP, α2δ-1 was efficiently expressed on the plasma membrane where it colocalized with PrP (Figures 6B, 6C, and 6K). In contrast, α2δ-1 was weakly expressed on the surface of PG14 PrP-expressing cells, and was mostly found in perinuclear patches where it colocalized with PrP (Figures 6E, 6F, and 6K), and with ER and Golgi markers (data not shown). This was seen in cells with high or low expression levels, ruling out that the abnormal localization of α2δ-1 was due to overexpression. The CaVα1A pore-forming subunit also accumulated intracellularly in PG14 PrP-expressing cells (Figures S6A–S6H), whereas there was no effect on the localization of 5′ nucleotidase (5′NT), a raft-resident GPI-anchored protein that does not belong to the VGCC complex (Davies et al., 2010) (Figures S6I–S6P). In cells expressing PG14/ΔHC PrP, α2δ-1 was more efficiently delivered to the cell surface, indicating that intracellular retention of mutant PrP played a role in the trafficking defect (Figures 6H, 6I, and 6K).

, 2008; Lerner et al , 2011) In regions nearer to the sensory pe

, 2008; Lerner et al., 2011). In regions nearer to the sensory periphery, cortical activity is reliably modulated by instantaneous physical parameters (e.g., the acoustics of a word), DNA Damage inhibitor but processing is largely independent of temporal context (e.g., whether that word occurs in a meaningful sentence). These more peripheral regions have been said to have short “temporal receptive windows” (TRWs). Further up the processing hierarchy, more and more of the sensory history is found to affect processing in the present moment. In areas with especially “long TRWs,” such as the temporoparietal junction, the cortical activity at each moment may depend on information that arrived over prior tens

of seconds. In this study, we aimed to map the large-scale topography of TRWs using electrocorticographic (ECoG) recording of the human brain. We further CB-839 in vivo asked whether regions with longer TRWs have distinctive properties in their population dynamics, which may be important for their capacity to accumulate information over long timescales. In particular, we hypothesized that slow components of neuronal dynamics would be more evident

in regions with long TRWs, relative to regions with short TRWs. We tested this hypothesis by performing ECoG recordings from the cerebral cortex of humans watching intact and scrambled audiovisual movie clips (Figure 1A). In quantifying local neuronal dynamics, we measured multiple signal components, but focused on fluctuations of power within the broad high-frequency range of 64–200 Hz. Human and monkey electrophysiology suggest that power fluctuations in the 64–200 Hz band are a distinct phenomenon from the γ oscillations found in visual cortices, and that shifts in this nonrhythmic broadband component index the population spike rate near an electrode (Crone et al., 2011; Manning et al., 2009; Miller, 2010; Nir et al., 2007; Ray and Maunsell, 2011; Whittingstall and Logothetis, 2009). Thus, when we mention fast or slow components of neuronal population dynamics, we are referring to

faster and slower Thymidine kinase fluctuations of broadband high-frequency power, which indexes the population spike rate. By measuring the ECoG responses to intact and scrambled movie clips, we confirmed, first, the presence of shorter TRWs in more sensory areas, and longer TRWs in higher order perceptual and cognitive cortices. Second, we observed that regions with long TRWs exhibit relatively more slow (<0.1 Hz) fluctuations of high-frequency power for both intact and scrambled movie clips. Third, we observed that these slow fluctuations of power were modulated with reliable time courses across repeated presentations of the movie. The slow fluctuations were more reliable for the intact than for the scrambled movie, suggesting that they may be connected to the processing of information over long timescales. We measured neural responses to stimuli with intact information and with scrambled information structure.