Frequency dependence of signal power and spatial reach of the local field potential

The first recording of electrical potential from brain activity was reported already in 1875, but still the interpretation of the signal is debated. To take full advantage of the new generation of microelectrodes with hundreds or even thousands of electrode contacts, an accurate quantitative link between what is measured and the underlying neural circuit activity is needed. Here we address the question of how the observed frequency dependence of recorded local field potentials (LFPs) should be interpreted. By use of a well-established biophysical modeling scheme, combined with detailed reconstructed neuronal morphologies, we find that correlations in the synaptic inputs onto a population of pyramidal cells may significantly boost the low-frequency components of the generated LFP. We further find that these low-frequency components may be less `local' than the high-frequency LFP components in the sense that (1) the size of signal-generation region of the LFP recorded at an electrode is larger and (2) that the LFP generated by a synaptically activated population spreads further outside the population edge due to volume conduction

Identification of functional p53-binding motifs in the mouse wig-1 promoter

AbstractWe previously identified wig-1 as a p53-induced mouse gene that encodes a nuclear zinc finger protein with unknown function. To investigate whether wig-1 is a direct target of p53-dependent transactivation, a DNA fragment corresponding to the promoter region was cloned and sequenced. Three regions containing consensus p53-binding sites were identified. Two p53-binding motifs formed DNA–protein complexes with p53 and were able to drive p53-dependent transcription in a luciferase reporter assay. Our results demonstrate that wig-1 is a direct target of p53-mediated transcriptional transactivation

Drilling of shallow marine sulfide-sulfate mineralisation in south-eastern Tyrrhenian Sea, Italy; Seafloor sulfides, Tyrrhenian Sea, highsulfidation; hydrothermal systems, Palinuro

Semi-massive to massive sulfides with abundant late native sulfur were drilled in a shallowwater hydrothermal system in an island arc volcanic setting at the Palinuro volcanic complex in the Tyrrhenian Sea, Italy. Overall, 12.7 m of sulfide mineralisation were drilled in a sediment-filled depression at a water depth of 630 - 650 m using the lander-type Rockdrill I drill rig of the British Geological Survey. Polymetallic (Zn, Pb, Sb, As, Ag) sulfides overlie massive pyrite. The massive sulfide mineralisation contains a number of atypical minerals, including enargite-famatinite, tennantite-tetrahedrite, stibnite, bismuthinite, and Pb-,Sb-, and Ag-sulfosalts, that do not commonly occur in mid-ocean ridge massive sulfides. Analogous to subaerial epithermal deposits, the occurrence of these minerals and the presence of abundant native sulfur suggest an intermediate to high sulfidation and/or high oxididation state of the hydrothermal fluids in contrast to the near-neutral and reducing fluids from which base metal-rich massive sulfides along mid-ocean ridges typically form. Oxidised conditions during sulfide deposition are likely related to the presence of magmatic volatiles in the mineralising fluids that were derived from a degassing magma chamber below the Palinuro volcanic complex

High-frequency Electrocardiogram Analysis in the Ability to Predict Reversible Perfusion Defects during Adenosine Myocardial Perfusion Imaging

Background: A previous study has shown that analysis of high-frequency QRS components (HF-QRS) is highly sensitive and reasonably specific for detecting reversible perfusion defects on myocardial perfusion imaging (MPI) scans during adenosine. The purpose of the present study was to try to reproduce those findings. Methods: 12-lead high-resolution electrocardiogram recordings were obtained from 100 patients before (baseline) and during adenosine Tc-99m-tetrofosmin MPI tests. HF-QRS were analyzed regarding morphology and changes in root mean square (RMS) voltages from before the adenosine infusion to peak infusion. Results: The best area under the curve (AUC) was found in supine patients (AUC=0.736) in a combination of morphology and RMS changes. None of the measurements, however, were statistically better than tossing a coin (AUC=0.5). Conclusion: Analysis of HF-QRS was not significantly better than tossing a coin for determining reversible perfusion defects on MPI scans

Electrodiffusive model for astrocytic and neuronal ion concentration dynamics

Electrical neural signalling typically takes place at the time-scale of milliseconds, and is typically modeled using the cable equation. This is a good approximation for processes when ionic concentrations vary little during the time course of a simulation. During periods of intense neural signalling, however, the local extracellular K+ concentration may increase by several millimolars. Clearance of excess K+ likely depends partly on diffusion in the extracellular space, partly on local uptake by- and intracellular transport within astrocytes. This process takes place at the time scale of seconds, and can not be modeled accurately without accounting for the spatiotemporal variations in ion concentrations. The work presented here consists of two main parts: First, we developed a general electrodiffusive formalism for modeling ion concentration dynamics in a one-dimensional geometry, including both an intra- and extracellular domain. The formalism was based on the Nernst-Planck equations. It ensures (i) consistency between the membrane potential and ion concentrations, (ii) global particle/charge conservation, and (iii) accounts for diffusion and concentration dependent variations in resistivities. Second, we applied the formalism to model how astrocytes exchange ions with the ECS, and identified the key astrocytic mechanisms involved in K+ removal from high concentration regions. We found that a local increase in extracellular K\textsuperscript{+} evoked a local depolarization of the astrocyte membrane, which at the same time (i) increased the local astrocytic uptake of K\textsuperscript{+}, (ii) suppressed extracellular transport of K+, (iii) increased transport of K+ within astrocytes, and (iv) facilitated astrocytic relase of K+ in extracellular low concentration regions. In summary, these mechanisms seem optimal for shielding the extracellular space from excess K+.Comment: 19 pages, 5 figures, 1 table (Equations 37 & 38 and the two first equations in Figure 2 were corrected May 30th 2013