736 research outputs found
Comment on ``Critical branching captures activity in living neural networks and maximizes the number of metastable states''
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
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
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
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.
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
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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