Topic
Epileptogenesis
About: Epileptogenesis is a research topic. Over the lifetime, 4218 publications have been published within this topic receiving 170809 citations.
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TL;DR: The transient manifestation of strong NMDA receptor-mediated potentials coincides temporally with a 'developmental window' within which there is enhanced sensitivity for epileptogenesis and for induction of long-term synaptic modifications in rat cortex.
95 citations
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TL;DR: The in vitro changes in synaptic potentials that occur in neurons of the basolateral amygdala 4-6 weeks after kindling suggest that the amygdala is an area of the brain particularly sensitive to epileptogenesis.
95 citations
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TL;DR: The pilocarpine model of epilepsy is used to demonstrate that regulation of excitatory synaptic drive onto GABAergic interneurons is impaired during epileptogenesis, and results indicate that, in the SE-experienced rat, exciteatory drive to hilar border inhibitory interneurs is weakened through a use-dependent mechanism involving group II metabotropic glutamate receptors.
Abstract: Impaired GABAergic inhibition may contribute to the development of hyperexcitability in epilepsy. We used the pilocarpine model of epilepsy to demonstrate that regulation of excitatory synaptic drive onto GABAergic interneurons is impaired during epileptogenesis. Synaptic input from granule cells (GCs), perforant path, and CA3 inputs onto hilar border interneurons of the dentate gyrus were examined in rat hippocampal slices during the latent period (1-8 d) after induction of status epilepticus (SE). Short-term depression (STD) of GC inputs to interneurons induced by brief (500-800 msec), repetitive (5-20 Hz) stimulation, as well as paired-pulse depression at both GC and CA3 inputs to interneurons, were significantly (p < 0.05) enhanced in SE-experienced rats. In contrast, we found no significant differences between SE-experienced and age-matched control rats in the properties of minimal EPSCs evoked at low frequency (0.3 Hz). Consistent with reduced GABAergic inhibition onto granule cells, paired-pulse depression of perforant path-evoked granule cell population spikes was lost in SE-experienced rats. Enhanced STD was partially mediated by group II metabotropic glutamate receptors, because the selective antagonist, 2S-2-amino-2-(1S,2S-2-carboxycyclopropyl-1-yl)-3-(xanth-9-yl)propanoic acid, attenuated STD in SE-experienced rats but had no effect on STD of GC inputs in the normal adult rat. The group II mGluR agonist, (2S',1R',2R',3R')-2-(2,3-dicarboxylcyclopropyl) glycine (1 micrometer), produced a greater depression of GC input to hilar border interneurons in SE-experienced rats than in controls. These results indicate that, in the SE-experienced rat, excitatory drive to hilar border inhibitory interneurons is weakened through a use-dependent mechanism involving group II metabotropic glutamate receptors.
95 citations
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TL;DR: The "latent period" is suggested to be a state of "epileptic maturation," rather than a prolonged period of "Epileptogenesis," and therefore the antiepileptogenic therapeutic window may only remain open during the first week after injury, when some delayed cell death may still be preventable.
95 citations
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TL;DR: Those miRNAs that are altered in plasma before the first spontaneous seizure, like miR-9a-3p, may be proposed as putative biomarkers of epileptogenesis.
Abstract: The identification of biomarkers of the transformation of normal to epileptic tissue would help to stratify patients at risk of epilepsy following brain injury, and inform new treatment strategies. MicroRNAs (miRNAs) are an attractive option in this direction. In this study, miRNA microarrays were performed on laser-microdissected hippocampal granule cell layer (GCL) and on plasma, at different time points in the development of pilocarpine-induced epilepsy in the rat: latency, first spontaneous seizure and chronic epileptic phase. Sixty-three miRNAs were differentially expressed in the GCL when considering all time points. Three main clusters were identified that separated the control and chronic phase groups from the latency group and from the first spontaneous seizure group. MiRNAs from rats in the chronic phase were compared to those obtained from the laser-microdissected GCL of epileptic patients, identifying several miRNAs (miR-21-5p, miR-23a-5p, miR-146a-5p and miR-181c-5p) that were up-regulated in both human and rat epileptic tissue. Analysis of plasma samples revealed different levels between control and pilocarpine-treated animals for 27 miRNAs. Two main clusters were identified that segregated controls from all other groups. Those miRNAs that are altered in plasma before the first spontaneous seizure, like miR-9a-3p, may be proposed as putative biomarkers of epileptogenesis.
95 citations