736 research outputs found

    Comment on ``Critical branching captures activity in living neural networks and maximizes the number of metastable states''

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    It is shown that, contrary to the claims in a recent letter by Haldeman and Beggs (PRL, 94, 058101, 2005), the branching ratio in epileptic cortical cultures is smaller than one. In addition, and also in contrast to claims made in that paper, the number of metastable states is not significantly different between cortical cultures in the critical state and cultures made epileptic using picrotoxin.Comment: Submitted Comment to PR

    Decline of long-range temporal correlations in the human brain during sustained wakefulness

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    Sleep is crucial for daytime functioning, cognitive performance and general well-being. These aspects of daily life are known to be impaired after extended wake, yet, the underlying neuronal correlates have been difficult to identify. Accumulating evidence suggests that normal functioning of the brain is characterized by long-range temporal correlations (LRTCs) in cortex, which are supportive for decision-making and working memory tasks. Here we assess LRTCs in resting state human EEG data during a 40-hour sleep deprivation experiment by evaluating the decay in autocorrelation and the scaling exponent of the detrended fluctuation analysis from EEG amplitude fluctuations. We find with both measures that LRTCs decline as sleep deprivation progresses. This decline becomes evident when taking changes in signal power into appropriate consideration. Our results demonstrate the importance of sleep to maintain LRTCs in the human brain. In complex networks, LRTCs naturally emerge in the vicinity of a critical state. The observation of declining LRTCs during wake thus provides additional support for our hypothesis that sleep reorganizes cortical networks towards critical dynamics for optimal functioning

    Universal Organization of Resting Brain Activity at the Thermodynamic Critical Point

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    Thermodynamic criticality describes emergent phenomena in a wide variety of complex systems. In the mammalian brain, the complex dynamics that spontaneously emerge from neuronal interactions have been characterized as neuronal avalanches, a form of critical branching dynamics. Here, we show that neuronal avalanches also reflect that the brain dynamics are organized close to a thermodynamic critical point. We recorded spontaneous cortical activity in monkeys and humans at rest using high-density intracranial microelectrode arrays and magnetoencephalography, respectively. By numerically changing a control parameter equivalent to thermodynamic temperature, we observed typical critical behavior in cortical activities near the actual physiological condition, including the phase transition of an order parameter, as well as the divergence of susceptibility and specific heat. Finite-size scaling of these quantities allowed us to derive robust critical exponents highly consistent across monkey and humans that uncover a distinct, yet universal organization of brain dynamics

    The interplay between long- and short-range temporal correlations shapes cortex dynamics across vigilance states

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    Increasing evidence suggests that cortical dynamics during wake exhibits long-range temporal correlations suitable to integrate inputs over extended periods of time to increase the signal-to-noise ratio in decision-making and working memory tasks. Accordingly, sleep has been suggested as a state characterized by a breakdown of long-range correlations; detailed measurements of neuronal timescales that support this view, however, have so far been lacking. Here we show that the long timescales measured at the individual neuron level in freely-behaving rats during the awake state are abrogated during non-REM (NREM) sleep. We provide evidence for the existence of two distinct states in terms of timescale dynamics in cortex: one which is characterized by long timescales which dominate during wake and REM sleep, and a second one characterized by the absence of long-range temporal correlations which characterizes NREM sleep. We observe that both timescale regimes can co-exist and, in combination, lead to an apparent gradual decline of long timescales during extended wake which is restored after sleep. Our results provide a missing link between the observed long timescales in individual neuron fluctuations during wake and the reported absence of long-term correlations during deep sleep in EEG and fMRI studies. They furthermore suggest a network-level function of sleep, to reorganize cortical networks towards states governed by slow cortex dynamics to ensure optimal function for the time awake

    Npp1 promotes atherosclerosis in ApoE knockout mice.

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    Ecto-nucleotide pyrophosphatase/phosphodiesterase 1 (NPP1) generates inorganic pyrophosphate (PP(i)), a physiologic inhibitor of hydroxyapatite deposition. In a previous study, we found NPP1 expression to be inversely correlated with the degree of atherosclerotic plaque calcification. Moreover, function-impairing mutations of ENPP1, the gene encoding for NPP1, are associated with severe, artery tunica media calcification and myointimal hyperplasia with infantile onset in human beings. NPP1 and PP(i) have the potential to modulate atherogenesis by regulating arterial smooth muscle cell (SMC) differentiation and function, including increase of pro-atherogenic osteopontin (OPN) expression. Hence, this study tested the hypothesis that NPP1 deficiency modulates both atherogenesis and atherosclerotic intimal plaque calcification. Npp1/ApoE double deficient mice were generated by crossing mice bearing the ttw allele of Enpp1 (that encodes a truncation mutation) with ApoE null mice and fed with high-fat/high-cholesterol atherogenic diet. Atherosclerotic lesion area and calcification were examined at 13, 18, 23 and 28 weeks of age. The aortic SMCs isolated from both ttw/ttw ApoE(-/-) and ttw/+ ApoE(-/-) mice demonstrated decreased Opn expression. The 28-week-old ttw/ttw ApoE(-/-) and ttw/+ ApoE(-/-) had significantly smaller atherosclerotic lesions compared with wild-type congenic ApoE(-/-) mice. Only ttw/ttw but not ttw/+ mice developed artery media calcification. Furthermore in ttw/+ mice, there was a tendency towards increased plaque calcification compared to ApoE(-/-) mice without Npp1 deficiency. We conclude that Npp1 promotes atherosclerosis, potentially mediated by Opn expression in ApoE knockout mice

    Neutral theory and scale-free neural dynamics

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    Avalanches of electrochemical activity in brain networks have been empirically reported to obey scale-invariant behavior --characterized by power-law distributions up to some upper cut-off-- both in vitro and in vivo. Elucidating whether such scaling laws stem from the underlying neural dynamics operating at the edge of a phase transition is a fascinating possibility, as systems poised at criticality have been argued to exhibit a number of important functional advantages. Here we employ a well-known model for neural dynamics with synaptic plasticity, to elucidate an alternative scenario in which neuronal avalanches can coexist, overlapping in time, but still remaining scale-free. Remarkably their scale-invariance does not stem from underlying criticality nor self-organization at the edge of a continuous phase transition. Instead, it emerges from the fact that perturbations to the system exhibit a neutral drift --guided by demographic fluctuations-- with respect to endogenous spontaneous activity. Such a neutral dynamics --similar to the one in neutral theories of population genetics-- implies marginal propagation of activity, characterized by power-law distributed causal avalanches. Importantly, our results underline the importance of considering causal information --on which neuron triggers the firing of which-- to properly estimate the statistics of avalanches of neural activity. We discuss the implications of these findings both in modeling and to elucidate experimental observations, as well as its possible consequences for actual neural dynamics and information processing in actual neural networks.Comment: Main text: 8 pages, 3 figures. Supplementary information: 5 pages, 4 figure
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