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Potential Oscillations (potential + oscillation)
Selected AbstractsCalmodulin kinase II initiates arrhythmogenicity during metabolic acidification in murine heartsACTA PHYSIOLOGICA, Issue 1 2009T. H. Pedersen Abstract Aim:, The multifunctional signal molecule calmodulin kinase II (CaMKII) has been associated with cardiac arrhythmogenesis under conditions where its activity is chronically elevated. Recent studies report that its activity is also acutely elevated during acidosis. We test a hypothesis implicating CaMKII in the arrhythmogenesis accompanying metabolic acidification. Methods:, We obtained monophasic action potential recordings from Langendorff-perfused whole heart preparations and single cell action potentials (AP) using whole-cell patch-clamped ventricular myocytes. Spontaneous sarcoplasmic reticular (SR) Ca2+release events during metabolic acidification were investigated using confocal microscope imaging of Fluo-4-loaded ventricular myocytes. Results:, In Langendorff-perfused murine hearts, introduction of lactic acid into the Krebs-Henseleit perfusate resulted in abnormal electrical activity and ventricular tachycardia. The CaMKII inhibitor, KN-93 (2 ,m), reversibly suppressed this spontaneous arrhythmogenesis during intrinsic rhythm and regular 8 Hz pacing. However, it failed to suppress arrhythmia evoked by programmed electrical stimulation. These findings paralleled a CaMKII-independent reduction in the transmural repolarization gradients during acidosis, which previously has been associated with the re-entrant substrate under other conditions. Similar acidification produced spontaneous AP firing and membrane potential oscillations in patch-clamped isolated ventricular myocytes when pipette solutions permitted cytosolic Ca2+ to increase following acidification. However, these were abolished by both KN-93 and use of pipette solutions that held cytosolic Ca2+ constant during acidosis. Acidosis also induced spontaneous Ca2+ waves in isolated intact Fluo-4-loaded myocytes studied using confocal microscopy that were abolished by KN-93. Conclusion:, These findings together implicate CaMKII-dependent SR Ca2+ waves in spontaneous arrhythmic events during metabolic acidification. [source] Cooling Abolishes Neuronal Network Synchronization in Rat Hippocampal SlicesEPILEPSIA, Issue 6 2002Sam P. Javedan Summary: ,Purpose: We sought to determine whether cooling brain tissue from 34 to 21°C could abolish tetany-induced neuronal network synchronization (gamma oscillations) without blocking normal synaptic transmission. Methods: Intracellular and extracellular electrodes recorded activity in transverse hippocampal slices (450,500 ,m) from Sprague,Dawley male rats, maintained in an air,fluid interface chamber. Gamma oscillations were evoked by afferent stimulation at 100 Hz for 200 ms. Baseline temperature in the recording chamber was 34°C, reduced to 21°C within 20 min. Results: Suprathreshold tetanic stimuli evoked membrane potential oscillations in the 40-Hz frequency range (n = 21). Gamma oscillations induced by tetanic stimulation were blocked by bicuculline, a ,-aminobutyric acid (GABA)A -receptor antagonist. Cooling from 34 to 21°C reversibly abolished gamma oscillations in all slices tested. Short, low-frequency discharges persisted after cooling in six of 14 slices. Single-pulse,evoked potentials, however, were preserved after cooling in all cases. Latency between stimulus and onset of gamma oscillation was increased with cooling. Frequency of oscillation was correlated with chamber cooling temperature (r = 0.77). Tetanic stimulation at high intensity elicited not only gamma oscillation, but also epileptiform bursts. Cooling dramatically attenuated gamma oscillation and abolished epileptiform bursts in a reversible manner. Conclusions: Tetany-induced neuronal network synchronization by GABAA -sensitive gamma oscillations is abolished reversibly by cooling to temperatures that do not block excitatory synaptic transmission. Cooling also suppresses transition from gamma oscillation to ictal bursting at higher stimulus intensities. These findings suggest that cooling may disrupt network synchrony necessary for epileptiform activity. [source] Spindles-Inducing Mechanism Modulates Sleep Activation of Interictal Epileptiform Discharges in the Landau,Kleffner SyndromeEPILEPSIA, Issue 2 2000L. Nobili Summary: Purpose: Landau,Kleffner syndrome (LKS) is characterized by a marked increase of interictal epileptiform discharges (IEDs) during sleep. During nonrapid eye movement (NREM) sleep, neuronal membrane potential oscillations lead to the appearance of spindles and delta waves in the surface EEG and might develop into paroxysmal synchronization. Spectral analysis allows the quantitative description of the dynamics of delta (slow-wave activity, SWA, 0.5-4.5 Hz) and sigma activity (SA, 12.0,16.0 Hz) and can be used to assess the relation between SA, SWA, and IEDs during sleep. Methods: We performed six overnight continuous EEG-polysomnographic studies in three patients with LKS. The temporal series of SWA and SA were obtained from a spike-free derivation lead. The IEDs count was performed on the most active lead. Relations between sigma and SWA and time series of lEDs were tested by means of correlation techniques after data normalization. Results: Our results revealed a significantly higher correlation between IEDs and SA with respect to SWA in all the subjects, in total sleep time. The same analysis limited to NREM sleep highlights the better correlation between SA and IEDs. Conclusions: Our data suggest that neural mechanisms involved in the generation of sleep spindles facilitate IEDs production in LKS. [source] Comparison of spatial integration and surround suppression characteristics in spiking activity and the local field potential in macaque V1EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2008M. A. Gieselmann Abstract Neurons in primary visual cortex exhibit well documented centre,surround receptive field organization, whereby the centre is dominated by excitatory influences and the surround is generally dominated by inhibitory influences. These effects have largely been established by measuring the output of neurons, i.e. their spiking activity. How excitation and inhibition are reflected in the local field potential (LFP) is little understood. As this can bear on the interpretation of human fMRI BOLD data and on our understanding of the mechanisms of local field potential oscillations, we measured spatial integration and centre,surround properties in single- and multiunit recordings of V1 in the awake fixating macaque monkey, and compared these to spectral power in different frequency bands of simultaneously recorded LFPs. We quantified centre,surround organization by determining the size of the summation and suppression area in spiking activity as well as in different frequency bands of the LFP, with the main focus on the gamma band. Gratings extending beyond the summation area usually inhibited spiking activity while the LFP gamma-band activity increased monotonically for all grating sizes. This increase was maximal for stimuli infringing upon the near classical receptive field surround, where suppression started to dominate spiking activity. Thus, suppressive influences in primary cortex can be inferred from spiking activity, but they also seem to affect specific features of gamma-band LFP activity. [source] Dynamic changes in the direction of the theta rhythmic drive between supramammillary nucleus and the septohippocampal systemHIPPOCAMPUS, Issue 6 2006Bernat Kocsis Abstract Neurons in the supramammillary nucleus (SUM) of urethane-anesthetized rats fire rhythmically in synchrony with hippocampal theta rhythm. As these neurons project to the septum and hippocampus, it is generally assumed that their role is to mediate ascending activation, leading to the hippocampal theta rhythm. However, the connections between SUM and the septohippocampal system are reciprocal; there is strong evidence that theta remains in the hippocampus after SUM lesions and in the SUM after lesioning the medial septum. The present study examines the dynamics of coupling between rhythmic discharge in the SUM and hippocampal field potential oscillations, using the directionality information carried by the two signals. Using directed transfer function analysis, we demonstrate that during sensory-elicited theta rhythm and also during short episodes of theta acceleration of spontaneous oscillations, the spike train of a subpopulation of SUM neurons contains information predicting future variations in rhythmic field potentials in the hippocampus. In contrast, during slow spontaneous theta rhythm, it is the SUM spike signal that can be predicted from the preceding segment of the electrical signal recorded in the hippocampus. These findings indicate that, in the anesthetized rat, SUM neurons effectively drive theta oscillations in the hippocampus during epochs of sensory-elicited theta rhythm and short episodes of theta acceleration, whereas spontaneous slow theta in the SUM is controlled by descending input from the septohippocampal system. Thus, in certain states, rhythmically firing SUM neurons function to accelerate the septal theta oscillator, and in others, they are entrained by a superordinate oscillatory network. © 2006 Wiley-Liss Inc. [source] Dynamical Complexity in Electrochemical Oxidations of ThiocyanateCHINESE JOURNAL OF CHEMISTRY, Issue 4 2009Li LIU Abstract Kinetics and mechanism of the electrochemical oxidation of thiocyanate on a Pt electrode were investigated by using various electrochemical methods, in which both current and potential oscillations have been observed. Cyclic voltammetry measurements illustrate that the oxidation process consists of two steps. In addition to the oscillatory behavior, the system also exhibits bistability, in which the oxidation could be switched between a high and a low current density states with a temporal potential perturbation. The presence of inert ions with stronger absorption also induces transitions from oscillatory to steady reactions in the thiocyanate system. [source] | ||||||||||