The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
To characterize a critically ill cohort with status epilepticus (SE) by the illness severity scoring systems SAPS II (Simplified Acute Physiology Score II), APACHE II (Acute Physiology and Chronic Health Evaluation II), and SOFA (Sequential Organ Failure Assessment), and to compare their performance with the STESS (Status Epilepticus Severity Score) for outcome prediction.
We describe a 7-week-old infant with tuberous sclerosis (TSC1 mutation) and hemimegalencephaly who underwent a functional hemispherectomy for status epilepticus.
The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
Following multivariate analysis, SE duration >12h (OR=3.266; 95%CI=1.077-9.908; p=0.037), STESS ≥3 (OR=4.816; 95%CI=1.435-16.165; p=0.011), and PFE (OR=3.526; 95%CI=1.184-10.506; p=0.024) were independently associated with a poor functional prognosis.
The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
The GABA<sub>B</sub> antagonist exhibited proconvulsant effect in P15 and P18SE as well as LiPAR rats returning the incidence of PTZ-induced seizures to values of control animals.
The polymorphism DRD4_VNTR was associated with family history of epilepsy (P = 0.003), DRD2_rs1800497 was related to status epilepticus (P = 0.022), and intron 8 VNTR DAT was related to higher seizure frequency (P = 0.019) and family history of epilepsy (P = 0.011).
However, GluR2 mRNAs bearing the long 3'-UTRs were shifted from untranslating mRNP complexes to ribosome-containing complexes after SE, pointing to a selective translational derepression of GluR2 mRNA mediated by the long 3'UTR.
CaMKII-dependent dendrite ramification and spine generation promote spatial training-induced memory improvement in a rat model of sporadic Alzheimer's disease.
The present study aimed to investigate the mRNA expression of excitatory amino acid transporters 1-3 (EAATs) and the subunits of the NMDA (GluN1, GluN2a, and GluN2b) and AMPA (GluA1 and GluA2) glutamate receptors following status epilepticus in a rat lithium-pilocarpine model.
In the present study, we divided pilocarpine-induced SE Wistar rats into three main groups: the TAT-GluA2NT1-3-2 peptide group, the TAT-GluA2NT-scram peptide group, and the normal saline group, and injected different doses of peptides stereotaxically into the hippocampus of SE rats to investigate whether the GluA2/GAPDH interaction could be disrupted by our TAT-GluA2NT1-3-2 peptide and determine its most appropriate dose.
H19 overexpression induced the activation of astrocytes and microglia and the release of proinflammatory cytokines (interleukin-1β and interleukin-6 and tumor necrosis factor-α) in the hippocampus, whereas H19 knockdown inhibited status epilepticus-induced glial cell activation.
Peroxisome proliferator-activated receptor gamma agonist, rosiglitazone, suppresses CD40 expression and attenuates inflammatory responses after lithium pilocarpine-induced status epilepticus in rats.
These findings suggest that SE-induced aberrant mitochondrial dynamics may be involved in translocation of active caspase-3 and HMGB1 into mitochondria, which regulate neuronal apoptosis and necrosis, respectively.