Moreover, these varied profiles of expression were differentially regulated following status epilepticus, with some increasing (Mash1, Id2), some falling (Hes5, Prox1), and others remaining mostly unchanged (NeuroD/BETA2, NeuroD2/NDRF, Id3, Rath2/Nex1).
Therefore, using the lithium-pilocarpine status epilepticus model, we performed a detailed in situ hybridization time-course study of five gp130 cytokines (interleukin [IL]-6, leukemia inhibitory factor [LIF], IL-11, oncostatin-m [OSM], and ciliary neurotrophic factor), gp130, and the receptors of the cytokines we found to be induced (IL-6 receptor [IL-6R], LIF receptor [LIF-R], and IL-11 receptor [IL-11R]).
Differential expression of suppressors of cytokine signaling-1, -2, and -3 in the rat hippocampus after seizure: implications for neuromodulation by gp130 cytokines.
In the present study, Pgp expression was studied by immunohistochemistry in rats 24 h after a status epilepticus induced by either pilocarpine or kainate, widely used models of temporal lobe epilepsy.
Expression of different isoforms of protein kinase C in the rat hippocampus after pilocarpine-induced status epilepticus with special reference to CA1 area and the dentate gyrus.
Hippocampal-parahippocampal protein expression of NCX1, 2, and 3, PMCA1-4, and NCKX2 at an early and late stage after kainate-induced status epilepticus (SE) was compared with that in control rats by using immunocytochemistry.
Our data demonstrated that the SE-induced increase in the expression of cleaved caspase 6 and its intraneuronal localization were dependent on the time delay from SE induction.
The spatiotemporal expression of ADAM9 and ADAM10 suggests that their regulation after the KA-induced status epilepticus could be related to neuroprotection.
The spatiotemporal expression of ADAM9 and ADAM10 suggests that their regulation after the KA-induced status epilepticus could be related to neuroprotection.