![]() The evidence is both positive and negative. In our view, the evidence that in vitro VFO is generated by gap junctional coupling between principal neurons is compelling. ![]() Clearer understanding of the two related issues-VFO spatiotemporal pattern and cellular mechanism-may have clinical importance: Factors in the brain that predispose to VFO may also predispose to seizures, or VFO itself may promote seizure onset. There also continues to be uncertainty concerning the cellular mechanisms of different sorts of VFOs and their significance for epileptogenesis ( Engel et al., 2009). To our knowledge, the detailed spatiotemporal patterns of VFOs have not yet been investigated. Simulation data are shown lower right: field potential of very fast network oscillation (above, spectral peak at 112 Hz), and simultaneous “intracellular recording” (below). The data in the gray box were expanded in the lower left: scale bars 0.2 mV, 40 mV, and 400 ms. ![]() The graph (right) shows pooled incidence plot (bin width 0.5 ms) for 500 field VFO periods with full spike data plotted as the gray line and spikelet data as the black line. The bath contained kainate, and alkaline artificial cerebrospinal fluid (aCSF) was pressure ejected onto the slice just before the trace begins. ( B) Upper traces are field and intracellular recordings (IB, or intrinsic bursting cell), showing VFO in layer 5 of rat temporal neocortex in “nonsynaptic conditions”: AMPA, N-methyl- d-aspartate (NMDA), and γ-aminobutyric acid (GABA) A receptors were, respectively, blocked with 21 SYM2206, AP5, and gabazine. ( A) Electrocorticography (ECoG) recording from epileptic frontal neocortex (previously unpublished data from patient B of Roopun et al., 2009). Very fast oscillations (VFOs) occur at the surface of human epileptic brain in layer 5 of rat neocortex, in vitro, with chemical synapses blocked and in a detailed network model of neurons coupled by gap junctions, without chemical synapses. These latter observations suggest that the ability to generate VFOs might be a normal facet of cortical function, which is pathologically enhanced in epilepsy. Although VFOs may be useful in identifying seizure-onset zones ( Roopun et al., 2009), it is interesting to note that VFO occurrence is not specific to particular pathologies, and it is not directly related to local pathologic changes ( Jacobs et al., 2008). ![]() 1 of Traub et al., 2001), and such activity presumably encompasses several squared centimeters of cortical surface. On different occasions, however, VFOs occur simultaneously in a number of subdural grid ECoG electrodes (e.g., Fig. Numerous authors have reported the occurrence of very fast field potential/electroencephalography (EEG)/electrocorticography (ECoG) oscillations, at frequencies ≥80 Hz, prior to, during, and after paroxysmal epileptic events (either interictal or ictal), and both in patients and in experimental preparations, in vivo and in vitro (references include, but are not limited to: Fisher et al., 1992 Bragin et al., 1999a, b, 2002 Grenier et al., 2001, 2003 Jacobs et al., 2008 Khosravani et al., 2009 Worrell et al., 2004 Traub 2et al., 2001, 2005 Roopun et al., in prep.) In some cases, VFOs appear to arise in exquisitely localized regions of cortical tissue ( Bragin et al., 1999b, 2002 Roopun et al., in 3prep.) sometimes other epileptiform events can also arise in highly localized regions ( Schevon et al., 2008).
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