Zero delay synchronization of chaos in coupled map lattices

We show that two coupled map lattices that are mutually coupled to one another with a delay can display zero delay synchronization if they are driven by a third coupled map lattice. We analytically estimate the parametric regimes that lead to synchronization and show that the presence of mutual delays enhances synchronization to some extent. The zero delay or isochronal synchronization is reasonably robust against mismatches in the internal parameters of the coupled map lattices and we analytically estimate the synchronization error bounds.Comment: 9 pages, 9 figures ; To appear in Phys. Rev.

Can distributed delays perfectly stabilize dynamical networks?

Signal transmission delays tend to destabilize dynamical networks leading to oscillation, but their dispersion contributes oppositely toward stabilization. We analyze an integro-differential equation that describes the collective dynamics of a neural network with distributed signal delays. With the gamma distributed delays less dispersed than exponential distribution, the system exhibits reentrant phenomena, in which the stability is once lost but then recovered as the mean delay is increased. With delays dispersed more highly than exponential, the system never destabilizes.Comment: 4pages 5figure

Neurophysiology

Contains research objectives and summary of research on sixteen research projects.National Institutes of Health (Grant 5 TO1 EY00090-03)National Institutes of Health (Grant 3 RO1 EY01149-03S1)Bell Laboratories (Grant)National Institutes of Health (Grant 5 RO1 NS12307-02)National Institutes of Health (Grant K04 NS00010

Neurophysiology

Contains research objectives and summary of research on seventeen research projects and reports on four research projects.National Institutes of Health (Grant 5 TOl EY00090-02)Bell Telephone Laboratories, Inc. (Grant)National Institutes of Health (Grant 5 ROI EY01149-03)National Institutes of Health (Grant NS 12307-01)National Institutes of Health (Grant 1 K04 NS00010

Neurophysiology

Contains reports on twenty research projects.Bell Laboratories (Grant)National Institutes of Health (Grant 5 R01 EY01149-03S2)National Institutes of Health (Grant 5 TO1 EY00090-04)National Institutes of Health (Grant 5 RO1 NS12307-03)National Institutes of Health (Grant K04 NS00010)National Multiple Sclerosis Society (Grant RG-1133-A-1)Health Sciences Fund (Grant 78-10

Transfer entropy—a model-free measure of effective connectivity for the neurosciences

Understanding causal relationships, or effective connectivity, between parts of the brain is of utmost importance because a large part of the brain’s activity is thought to be internally generated and, hence, quantifying stimulus response relationships alone does not fully describe brain dynamics. Past efforts to determine effective connectivity mostly relied on model based approaches such as Granger causality or dynamic causal modeling. Transfer entropy (TE) is an alternative measure of effective connectivity based on information theory. TE does not require a model of the interaction and is inherently non-linear. We investigated the applicability of TE as a metric in a test for effective connectivity to electrophysiological data based on simulations and magnetoencephalography (MEG) recordings in a simple motor task. In particular, we demonstrate that TE improved the detectability of effective connectivity for non-linear interactions, and for sensor level MEG signals where linear methods are hampered by signal-cross-talk due to volume conduction

Subliminal stimulation and somatosensory signal detection

Only a small fraction of sensory signals is consciously perceived. The brain's perceptual systems may include mechanisms of feedforward inhibition that protect the cortex from subliminal noise, thus reserving cortical capacity and conscious awareness for significant stimuli. Here we provide a new view of these mechanisms based on signal detection theory, and gain control. We demonstrated that subliminal somatosensory stimulation decreased sensitivity for the detection of a subsequent somatosensory input, largely due to increased false alarm rates. By delivering the subliminal somatosensory stimulus and the to-be-detected somatosensory stimulus to different digits of the same hand, we show that this effect spreads across the sensory surface. In addition, subliminal somatosensory stimulation tended to produce an increased probability of responding “yes”, whether the somatosensory stimulus was present or not. Our results suggest that subliminal stimuli temporarily reduce input gain, avoiding excessive responses to further small inputs. This gain control may be automatic, and may precede discriminative classification of inputs into signals or noise. Crucially, we found that subliminal inputs influenced false alarm rates only on blocks where the to-be-detected stimuli were present, and not on pre-test control blocks where they were absent. Participants appeared to adjust their perceptual criterion according to a statistical distribution of stimuli in the current context, with the presence of supraliminal stimuli having an important role in the criterion-setting process. These findings clarify the cognitive mechanisms that reserve conscious perception for salient and important signals

Control of somatosensory cortical processing by thalamic posterior medial nucleus: A new role of thalamus in cortical function

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Current knowledge of thalamocortical interaction comes mainly from studying lemniscal thalamic systems. Less is known about paralemniscal thalamic nuclei function. In the vibrissae system, the posterior medial nucleus (POm) is the corresponding paralemniscal nucleus. POm neurons project to L1 and L5A of the primary somatosensory cortex (S1) in the rat brain. It is known that L1 modifies sensory-evoked responses through control of intracortical excitability suggesting that L1 exerts an influence on whisker responses. Therefore, thalamocortical pathways targeting L1 could modulate cortical firing. Here, using a combination of electrophysiology and pharmacology in vivo, we have sought to determine how POm influences cortical processing. In our experiments, single unit recordings performed in urethane- anesthetized rats showed that POm imposes precise control on the magnitude and duration of supra- and infragranular barrel cortex whisker responses. Our findings demonstrated that L1 inputs from POm imposed a time and intensity dependent regulation on cortical sensory processing. Moreover, we found that blocking L1 GABAergic inhibition or blocking P/Q-type Ca2+ channels in L1 prevents POm adjustment of whisker responses in the barrel cortex. Additionally, we found that POm was also controlling the sensory processing in S2 and this regulation was modulated by corticofugal activity from L5 in S1. Taken together, our data demonstrate the determinant role exerted by the POm in the adjustment of somatosensory cortical processing and in the regulation of cortical processing between S1 and S2. We propose that this adjustment could be a thalamocortical gain regulation mechanism also present in the processing of information between cortical areas.This work was supported by a grant from Ministerio de Economia y Competitividad (BFU2012- 36107