Chemoconvulsants that induce status epilepticus in rodents have been widely used over the past decades due to their capacity to reproduce with high similarity neuropathological and electroencephalographic features observed in patients with temporal lobe epilepsy (TLE). Kainic acid is one of the most used chemoconvulsants in experimental models. KA administration mainly induces neuronal loss in the hippocampus. We focused the present review inthe c-Jun N-terminal kinase-signaling pathway (JNK), since it has been shown to play a key role in the process of neuronal death following KA activation. Among the three isoforms of JNK (JNK1, JNK2, JNK3), JNK3 is widely localized in the majority of areas of the hippocampus, whereas JNK1 levels are located exclusively in the CA3 and CA4 areas and in dentate gyrus. Disruption of the gene encoding JNK3 in mice renders neuroprotection to KA, since these animals showed a reduction in seizure activity and a diminution in hippocampal neuronal apoptosis. In light of this, JNK3 could be a promising subcellular target for future therapeutic interventions in epilepsy.
The basic layout of the vertebrate body is built during the initial stages of embryonic development by the sequential addition of new tissue as the embryo grows at its caudal end. During this process the neuro-mesodermal progenitors (NMPs) are thought to generate the postcranial neural tube and paraxial mesoderm. In recent years, several approaches have been designed to determine the NMP molecular fingerprint but a simple method to isolate them from embryos without the need of transgenic markers is still missing. We wanted to identify a suitable cell surface marker allowing isolation of NMPs from the embryo without the need of previous genetic modifications. We used a genetic strategy to recover NMPs on the basis of their ability to populate the tail bud and searched their transcriptome for cell surface markers specifically enriched in these cells. We found a distinct Epha1 expression profile in progenitor-containing areas of the mouse embryo, consisting in at least two subpopulations of Epha1-positive cells according to their Epha1 expression levels. We show that double Sox2/T(Bra) positive cells are preferentially associated with the Epha1 High compartment, indicating that NMPs might be contained within this cell pool. Transcriptional profiling of Epha1-positive tail bud cells also showed enrichment of Epha1 High cells in known NMP markers. Interestingly, the Epha1 Low compartment contains a molecular signature compatible with notochord progenitor identity. Our results thus indicate that Epha1 could represent a valuable cell surface marker for different subsets of mouse embryonic axial progenitors. 3 INTRODUCTION
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