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EEG Oscillations (eeg + oscillation)

Distribution by Scientific Domains

Life Sciences	75%

Selected Abstracts

A Possible Role for Gap Junctions in Generation of Very Fast EEG Oscillations Preceding the Onset of, and Perhaps Initiating, Seizures

EPILEPSIA, Issue 2 2001
Roger D. Traub
Summary: ,Purpose: We propose an experimentally and clinically testable hypothesis, concerning the origin of very fast (>,70 Hz) EEG oscillations that sometimes precede the onset of focal seizures. These oscillations are important, as they may play a causal role in the initiation of seizures. Methods: Subdural EEG recordings were obtained from children with focal cortical dysplasias and intractable seizures. Intra- and extracellular recordings were performed in rat hippocampal slices, with induction of population activity, as follows: (a) bath-applied tetramethylamine (an intracellular alkalinizing agent, that opens gap junctions); (b) bath-applied carbachol, a cholinergic agonist; and (c) focal pressure ejection of hypertonic K+ solution. Detailed network simulations were performed, the better to understand the cellular mechanisms underlying oscillations. A major feature of the simulations was inclusion of axon,axon gap junctions between principal neurons, as supported by recent experimental data. Results: Very fast oscillations were found in children before seizure onset, but also superimposed on bursts during the seizure, and on interictal bursts. In slice experiments, very fast oscillations had previously been seen on interictal-like bursts; we now show such oscillations before, between, and after epileptiform bursts. Very fast oscillations were also seen superimposed on gamma (30,70 Hz) oscillations induced by carbachol or hypertonic K+, and in the latter case, very fast oscillations became continuous when chemical synapses were blocked. Simulations replicate these data, when axonal gap junctions are included. Conclusions: Electrical coupling between principal neurons, perhaps via axonal gap junctions, could underlie very fast population oscillations, in seizure-prone brain, but possibly also in normal brain. The anticonvulsant potential of gap-junction blockers such as carbenoxolone, now in clinical use for treatment of ulcer disease, should be considered. [source]

Changes in direct current (DC) potentials and infra-slow EEG oscillations at the onset of the luteinizing hormone (LH) pulse

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2000
Lisa Marshall
Abstract An essential function of the neuroendocrine system lies in the coordination of hypothalamo-pituitary secretory activity with neocortical neuronal activity. Cortical direct current (DC) potential shifts and EEG were monitored in conjunction with the circulating concentration of luteinizing hormone (LH) in humans while asleep to assess a hypothalamic,neocortical interaction. The onset of an LH pulse was accompanied (i) at frontocortical locations by a transient positive DC potential shift of ,,3 min duration and peak amplitude 50 ,V; (ii) at frontal and central locations by an increase in power of infra-slow EEG oscillations for periodicities between 64 and 320 s. Results uniquely demonstrate a coupling of hypothalamo-pituitary activity with regulation of neocortical excitability. [source]

Movement gating of beta/gamma oscillations involved in the N30 somatosensory evoked potential

HUMAN BRAIN MAPPING, Issue 5 2009
Ana Maria Cebolla
Abstract Evoked potential modulation allows the study of dynamic brain processing. The mechanism of movement gating of the frontal N30 component of somatosensory evoked potentials (SEP) produced by the stimulation of the median nerve at wrist remains to be elucidated. At rest, a power enhancement and a significant phase-locking of the electroencephalographic (EEG) oscillation in the beta/gamma range (25,35 Hz) are related to the emergence of the N30. The latter was also perfectly identified in presence of pure phase-locking situation. Here, we investigated the contribution of these rhythmic activities to the specific gating of the N30 component during movement. We demonstrated that concomitant execution of finger movement of the stimulated hand impinges such temporal concentration of the ongoing beta/gamma EEG oscillations and abolishes the N30 component throughout their large topographical extent on the scalp. This also proves that the phase-locking phenomenon is one of the main actors for the N30 generation. These findings could be explained by the involvement of neuronal populations of the sensorimotor cortex and other related areas, which are unable to respond to the phasic sensory activation and to phase-lock their firing discharges to the external sensory input during the movement. This new insight into the contribution of phase-locked oscillation in the emergence of the N30 and in its gating behavior calls for a reappraisal of fundamental and clinical interpretation of the frontal N30 component. Hum Brain Mapp 2009. © 2008 Wiley-Liss, Inc. [source]