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The response of the developing brain to epileptic seizures and to status epilepticus is highly age-specific. Neonates with their low cerebral metabolic rate and fragmentary neuronal networks can tolerate relatively prolonged seizures without suffering massive cell death, but severe seizures in experimental animals inhibit brain growth, modify neuronal(More)
PURPOSE We used a model of self-staining status epilepticus (SSSE), induced by brief intermittent stimulation of the perforant path in unanesthetized rats, to study the mechanism of initiation and of maintenance of SSSE and the role of neuropeptides in those processes. METHODS The perforant path was stimulated intermittently for 7 min (ineffective(More)
After 1h of lithium-pilocarpine status epilepticus (SE), immunocytochemical labeling of NMDA receptor NR1 subunits reveals relocation of subunits from the interior to the cell surface of dentate gyrus granule cells and CA3 pyramidal cells. Simultaneously, an increase in NMDA-miniature excitatory postsynaptic currents (mEPSC) as well as an increase in NMDA(More)
The mode and mechanism of neuronal death induced by status epilepticus (SE) in the immature brain have not been fully characterized. In this study, we analyzed the contribution of neuronal necrosis and caspase-3 activation to CA1 damage following lithium-pilocarpine SE in P14 rat pups. By electron microscopy, many CA1 neurons displayed evidence of early(More)
Omi/HtrA2 is a pro-apoptotic mitochondrial serine protease involved in caspase-dependent as well as caspase-independent cell death upon various brain injuries. However, the role of Omi/HtrA2 in neuronal death induced by status epilepticus (SE) in the immature brain has not been reported. In this study, we analyzed the contribution of serine protease(More)
We used a model of severe cholinergic status epilepticus (SE) to study polytherapy aimed at reversing the effects of seizure-induced loss of synaptic GABA(A) receptors and seizure-induced gain of synaptic NMDA receptors. Combinations of a benzodiazepine with ketamine and valproate, or with ketamine and brivaracetam, were more effective and less toxic than(More)
The mechanism of status epilepticus-induced neuronal death in the immature brain is not fully understood. In the present study, we examined the contribution of caspases in our lithium-pilocarpine model of status epilepticus in 14 days old rat pups. In CA1, upregulation of caspase-8, but not caspase-9, preceded caspase-3 activation in morphologically(More)
The neonatal brain has poorly developed GABAergic circuits, and in many of them GABA is excitatory, favoring ictogenicity. Frequently repeated experimental seizures impair brain development in an age-dependent manner. At critical ages, they delay developmental milestones, permanently lower seizure thresholds, and can cause very specific cognitive and(More)
During flurothyl seizures in 4-day-old rats, cortical concentration of ATP, phosphocreatine and glucose fell while lactate rose. Cortical energy use rate more than doubled, while glycolytic rate increased fivefold. Calculation of the cerebral metabolic balance during sustained seizures suggests that energy balance could be maintained in hyperglycemic(More)
There is considerable interest in defining the molecular pathways involved in seizure-induced neuronal death. Necrotic, apoptotic and anti-apoptotic signalling pathways are activated after status epilepticus (SE). Analyses of apoptosis and necrosis have been merely reported, however conditions of autophagic cell death with hallmarks of type 2 programmed(More)