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Sprouting and synaptogenesis of mossy fibers develop in adult hippocampus after epilepsy. In control conditions, mossy fibers constitute the main afferent pathway to the Ammon's horn, where they mainly innervate CA3 pyramidal cells, but after treatment with the convulsant agent, kainate, mossy fibers also innervate granule cell dendrites generating(More)
Kainic acid treatment (a model of temporal lobe epilepsy) induces Ammon's horn sclerosis, which is characterized by degeneration of CA3 pyramidal neurons and reactive gliosis. In the present study we have combined autoradiographic analysis of 3H-thymidine incorporation and immunocytochemistry to investigate this glial scarring phenomenon. The present(More)
Kainic acid treatment, a model of temporal lobe epilepsy, induces in CA3-CA4 fields of hippocampal complex a neuronal degeneration associated with glial hypertrophy and proliferation. After treatment with kainate, fibronectin (an extracellular matrix protein) immunoreactivity increases in CA3-CA4. Fibronectin antibodies stain proliferative cells(More)
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)
In the present report we describe the anatomical localization of cells expressing tenascin-C, an extracellular matrix glycoprotein, in the hippocampal complex of developing rats. We report a development-dependent down regulation of both tenascin-C protein and mRNA. The highest levels of expression of tenascin-C was observed in rat pups from embryonic day 18(More)
Seizures set in motion complex molecular and morphological changes in vulnerable structures, such as the hippocampal complex. A number of these changes are responsible for neuronal death of CA3 and hilar cells, which involves necrotic and apoptotic mechanisms. In surviving dentate granule cells seizures induce an increased expression of tubulin subunits and(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)
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)
Temporal lobe epilepsy is associated with neuronal death, gliosis and sprouting of mossy fibres in the hippocampus of human and rats. In the present study we show that immunoreactivity for tenascin-C (an extracellular matrix glycoprotein) increase in the hippocampus of epileptic rats. However, this increase was only observed in the cases displaying neuronal(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)