Radiation patterns of seismic surface waves from buried dipolar point sources in a flat stratified Earth

Explicit compact expressions were obtained for the far displacement field of Rayleigh and Love waves generated by force configurations which served to simulate shear-type faults with arbitrary dip and slip. The medium transfer functions for dipolar sources were computed for a Gutenberg flat continental earth model with 23 layers. These were then used to obtain universal radiation pattern charts for couple- and double-couple-type sources at various depths over the period range 50 to 350 sec. It was demonstrated by means of few typical examples that the radiation patterns of Rayleigh waves may depend strongly on the depth of the source, and unlike the fundamental Love mode may be rather sensitive to small variations in frequency. For a given source and frequency the radiation pattern may differ considerably from one mode to another

Fast evaluation of source parameters from isolated surface-wave signals. Part I. Universal tables

Tables for spectral displacements of seismic surface waves from shear dislocations in flat multilayered earth models were prepared. Earth response functions for seven modes (R_(11), R_(21), R_(12), L_0, L_1, L_2, L_3) at six periods (300 sec, 250 sec, 200 sec, 150 sec, 100 sec, 50 sec) and three paths (continental, oceanic, shield) were calculated for the source-depth range of 10 to 600 km at intervals of 5 km until 200 km, and thereafter at intervals of 10 km. Ground motion is given in micron-seconds for the three fundamental shear dislocations, each of strength U_0dS = 10^3 (m × km^2) and a delta-function time-dependence. The tables provide the means for rapid evaluation of source parameters from spectral radiation patterns of amplitudes and initial phases

Determination of source parameters by amplitude equalization of seismic surface waves: 2. Release of tectonic strain by underground nuclear explosions and mechanisms of earthquakes

The radiation patterns of Love and Rayleigh waves from three nuclear explosions (Hardhat, Haymaker, and Shoal) are studied to determine the nature of the asymmetry of radiation and the mechanism of Love wave generation. From a comparative study of different explosions it is reasoned that the Love waves are generated at the source of the explosion. The source function, represented as the superimposition of an isotropic dilatational component due to the explosion and a multipolar component due to the release of tectonic strain energy, is consistent with the observed radiation patterns and the amplitude spectrums. The amount of seismic energy due to the strain release is computed. In some cases (Haymaker and Shoal) it is found that this energy may be due to the relaxation of the pre-stressed medium by the explosion-formed cavity. In the case of Hardhat it is concluded that the explosion must have triggered some other strain release mechanism, such as an earthquake. The amplitude equalization method is applied to surface waves from an earthquake to determine the source parameters. From only the amplitude spectrums and radiation patterns of Love and Rayleigh waves, the source functions, source depth, strike and dip of the fault plane, and the rake of displacement are determined for the July 20, 1964, Fallon earthquake

Temporal coding at the immature depolarizing gabaergic synapse

In the developing hippocampus, GABA exerts depolarizing and excitatory actions and contributes to the generation of neuronal network driven giant depolarizing potentials (GDPs). Here, we studied spike time coding at immature GABAergic synapses and its impact on synchronization of the neuronal network during GDPs in the neonatal (postnatal days P2-6) rat hippocampal slices. Using extracellular recordings, we found that the delays of action potentials (APs) evoked by synaptic activation of GABA(A) receptors are long (mean, 65 ms) and variable (within a time window of 10-200 ms). During patch-clamp recordings, depolarizing GABAergic responses were mainly subthreshold and their amplification by persistent sodium conductance was required to trigger APs. AP delays at GABAergic synapses shortened and their variability reduced with an increase in intracellular chloride concentration during whole-cell recordings. Negative shift of the GABA reversal potential (EGABA) with low concentrations of bumetanide, or potentiation of GABA(A) receptors with diazepam reduced GDPs amplitude, desynchronized neuronal firing during GDPs and slowed down GDPs propagation. Partial blockade of GABA(A) receptors with bicuculline increased neuronal synchronization and accelerated GDPs propagation. We propose that spike timing at depolarizing GABA synapses is determined by intracellular chloride concentration. At physiological levels of intracellular chloride GABAergic depolarization does not reach the action potential threshold and amplification of GABAergic responses by non-inactivating sodium conductance is required for postsynaptic AP initiation. Slow and variable excitation at GABAergic synapse determines the level of neuronal synchrony and the rate of GDPs propagation in the developing hippocampus. © 2010 Valeeva, Abdullin, Tyzio, Skorinkin, Nikolski, Ben-Ari and Khazipov

Galanin Receptor 1 Deletion Exacerbates Hippocampal Neuronal Loss after Systemic Kainate Administration in Mice

Galanin is a neuropeptide with a wide distribution in the central and peripheral nervous systems and whose physiological effects are mediated through three G protein-coupled receptor subtypes, GalR1, GalR2, and GalR3. Several lines of evidence indicate that galanin, as well as activation of the GalR1 receptor, is a potent and effective modulator of neuronal excitability in the hippocampus.In order to test more formally the potential influence of GalR1 on seizure-induced excitotoxic cell death, we conducted functional complementation tests in which transgenic mice that exhibit decreased expression of the GalR1 candidate mRNA underwent kainate-induced status epilepticus to determine if the quantitative trait of susceptibility to seizure-induced cell death is determined by the activity of GalR1. In the present study, we report that reduction of GalR1 mRNA via null mutation or injection of the GalR1 antagonist, galantide, prior to kainate-induced status epilepticus induces hippocampal damage in a mouse strain known to be highly resistant to kainate-induced neuronal injury. Wild-type and GalR1 knockout mice were subjected to systemic kainate administration. Seven days later, Nissl and NeuN immune- staining demonstrated that hippocampal cell death was significantly increased in GalR1 knockout strains and in animals injected with the GalR1 antagonist. Compared to GalR1-expressing mice, GalR1-deficient mice had significantly larger hippocampal lesions after status epilepticus.Our results suggest that a reduction of GalR1 expression in the C57BL/6J mouse strain renders them susceptible to excitotoxic injury following systemic kainate administration. From these results, GalR1 protein emerges as a new molecular target that may have a potential therapeutic value in modulating seizure-induced cell death

Disinhibition of hippocampal CA3 neurons induced by suppression of an adenosine A1 receptor-mediated inhibitory tonus: Pre- and postsynaptic components

Intracellular recordings were performed on hippocampal CA3 neuronsin vitro to investigate the inhibitory tonus generated by endogenously produced adenosine in this brain region. Bath application of the highly selective adenosine A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine at concentrations up to 100 nM induced both spontaneous and stimulus-evoked epileptiform burst discharges. Once induced, the 1,3-dipropyl-8-cyclopentylxanthine-evoked epileptiform activity was apparently irreversible even after prolonged superfusion with drug-free solution. The blockade of glutamatergic excitatory synaptic transmission by preincubation of the slices with the amino-3-hydroxy-5-methyl-4-isoxazolpropionic acid receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (10 μM), but not with theN-methyl-d-aspartate receptor antagonistd-2-amino-5-phosphonovaleric acid (50/μM), prevented the induction of epileptiform activity by 1,3-dipropyl-8-cyclopentylxanthine. The generation of the burst discharges was independent of the membrane potential, and the amplitude of the slow component of the paroxysmal depolarization shift increased with hyperpolarization, indicating that the 1,3-dipropyl-8-cyclopentylxanthine-induced bursts were synaptically mediated events. Recordings from tetrodotoxin-treated CA3 neurons revealed a strong postsynaptic component of endogenous adenosinergic inhibition. Both 1,3-dipropyl-8-cyclopentylxanthine and the adenosine-degrading enzyme adenosine deaminase produced an apparently irreversible depolarization of the membrane potential by about 20 mV. Sometimes, this depolarization attained the threshold for the generation of putative calcium spikes, but no potential changes resembling paroxysmal depolarization shift-like events were observed

Efficient Symmetry Reduction and the Use of State Symmetries for Symbolic Model Checking

One technique to reduce the state-space explosion problem in temporal logic model checking is symmetry reduction. The combination of symmetry reduction and symbolic model checking by using BDDs suffered a long time from the prohibitively large BDD for the orbit relation. Dynamic symmetry reduction calculates representatives of equivalence classes of states dynamically and thus avoids the construction of the orbit relation. In this paper, we present a new efficient model checking algorithm based on dynamic symmetry reduction. Our experiments show that the algorithm is very fast and allows the verification of larger systems. We additionally implemented the use of state symmetries for symbolic symmetry reduction. To our knowledge we are the first who investigated state symmetries in combination with BDD based symbolic model checking

Intracellular chloride concentration influences the GABAA receptor subunit composition

GABAA receptors (GABAARs) exist as different subtype variants showing unique functional properties and defined spatio-temporal expression pattern. The molecular mechanisms underlying the developmental expression of different GABAAR are largely unknown. The intracellular concentration of chloride ([Cl−]i), the main ion permeating through GABAARs, also undergoes considerable changes during maturation, being higher at early neuronal stages with respect to adult neurons. Here we investigate the possibility that [Cl−]i could modulate the sequential expression of specific GABAARs subtypes in primary cerebellar neurons. We show that [Cl−]i regulates the expression of α3-1 and δ-containing GABAA receptors, responsible for phasic and tonic inhibition, respectively. Our findings highlight the role of [Cl−]i in tuning the strength of GABAergic responses by acting as an intracellular messenger

Brains swinging in concert: cortical phase synchronization while playing guitar

<p>Abstract</p> <p>Background</p> <p>Brains interact with the world through actions that are implemented by sensory and motor processes. A substantial part of these interactions consists in synchronized goal-directed actions involving two or more individuals. Hyperscanning techniques for assessing fMRI simultaneously from two individuals have been developed. However, EEG recordings that permit the assessment of synchronized neuronal activities at much higher levels of temporal resolution have not yet been simultaneously assessed in multiple individuals and analyzed in the time-frequency domain. In this study, we simultaneously recorded EEG from the brains of each of eight pairs of guitarists playing a short melody together to explore the extent and the functional significance of synchronized cortical activity in the course of interpersonally coordinated actions.</p> <p>Results</p> <p>By applying synchronization algorithms to intra- and interbrain analyses, we found that phase synchronization both within and between brains increased significantly during the periods of (i) preparatory metronome tempo setting and (ii) coordinated play onset. Phase alignment extracted from within-brain dynamics was related to behavioral play onset asynchrony between guitarists.</p> <p>Conclusion</p> <p>Our findings show that interpersonally coordinated actions are preceded and accompanied by between-brain oscillatory couplings. Presumably, these couplings reflect similarities in the temporal properties of the individuals' percepts and actions. Whether between-brain oscillatory couplings play a causal role in initiating and maintaining interpersonal action coordination needs to be clarified by further research.</p