1,721,110 research outputs found
A brief history on the oscillating roles of thalamus and cortex in absence seizures
No full textThis review summarizes the findings obtained over the past 70 years on the fundamental mechanisms underlying generalized spike-wave (SW) discharges associated with absence seizures. Thalamus and cerebral cortex are the brain areas that have attracted most of the attention from both clinical and experimental researchers. However, these studies have often favored either one or the other structure in playing a major role, thus leading to conflicting interpretations. Beginning with Jasper and Penfields topistic view of absence seizures as the result of abnormal functions in the so-called centrencephalon, we witness the naissance of a broader concept that considered both thalamus and cortex as equal players in the process of SW discharge generation. Furthermore, we discuss how recent studies have identified fine changes in cortical and thalamic excitability that may account for the expression of absence seizures in naturally occurring genetic rodent models and knockout mice. The end of this fascinating tale is presumably far from being written. However, I can confidently conclude that in the unfolding of this novel, we have discovered several molecular, cellular, and pharmacologic mechanisms that govern forebrain excitability, and thus consciousness, during the awake state and sleep
Mechanisms of epileptiform synchronization in cortical neuronal networks
No full textNeuronal synchronization supports different physiological states such as cognitive functions and sleep, and it is mirrored by identifiable EEG patterns ranging from gamma to delta oscillations. However, excessive neuronal synchronization is often the hallmark of epileptic activity in both generalized and partial epileptic disorders. Here, I will review the synchronizing mechanisms involved in generating epileptiform activity in the limbic system, which is closely involved in the pathophysiogenesis of temporal lobe epilepsy (TLE). TLE is often associated to a typical pattern of brain damage known as mesial temporal sclerosis, and it is one of the most refractory adult form of partial epilepsy. This epileptic disorder can be reproduced in animals by topical or systemic injection of pilocarpine or kainic acid, or by repetitive electrical stimulation; these procedures induce an initial status epilepticus and cause 1-4 weeks later a chronic condition of recurrent limbic seizures. Remarkably, a similar, seizure-free, latent period can be identified in TLE patients who suffered an initial insult in childhood and develop partial seizures in adolescence or early adulthood. Specifically, I will focus here on the neuronal mechanisms underlying three abnormal types of neuronal synchronization seen in both TLE patients and animal models mimicking this disorder: (i) interictal spikes; (ii) high frequency oscillations (80-500 Hz); and (iii) ictal (i.e., seizure) discharges. In addition, I will discuss the relationship between interictal spikes and ictal activity as well as recent evidence suggesting that specific seizure onsets in the pilocarpine model of TLE are characterized by distinctive patterns of spiking (also termed preictal) and high frequency oscillations
CA3-driven hippocampal-entorhinal loop controls rather than sustains in vitro limbic seizures.
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Volume-conducted epileptiform events between adjacent necortical slices in an interface tissue chamber
No full textFar-field" artifacts are presumed to contribute negligibly to the field potential activity recorded from brain slices maintained in vitro. While performing paired intracellular and field potential recordings from rat neocortical slices superfused with medium containing 4-aminopyridine + GABA receptor antagonists, we identified: (i) epileptiform discharges characterized by concomitant field oscillations (amplitude = 2.6-6.4 mV) and intracellular depolarizations as well as (ii) smaller amplitude (0.3-1.3 mV) field epileptiform events that were not associated with any intracellular activity. By placing an additional extracellular recording electrode into adjacent slices, we discovered that large amplitude, epileptiform discharges were generated concomitant to those seen in the first slice at the field potential level only. In addition, We found in these slices small amplitude, field discharges that were synchronous with those recorded intracellularly in the original slice. Analysis of the changes in field potential amplitude over space demonstrated that this parameter was reduced by approximately 60% when the recording electrode was moved from the slice generating the epileptiform activity to the bathing medium and further decreased in a quasi-linear mode when recordings were obtained from an adjacent slice. fit conclusion, these observations indicate that brain slices can, under appropriate conditions. produce field potentials that are of amplitude sufficient for being recorded from other slices in the tissue chamber. These findings suggest that caution should be taken in assuming that field potential activity seen in an in vitro brain slice is generated within the recorded tissue. (c) 2005 Elsevier B.V. All rights reserved
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