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Niquet J.,University of California at Los Angeles | Niquet J.,Epilepsy Research Laboratory 151 | Baldwin R.,Epilepsy Research Laboratory 151 | Gezalian M.,Epilepsy Research Laboratory 151 | And 2 more authors.
Epilepsy and Behavior | Year: 2015

In a rat model of status epilepticus (SE) induced by lithium and pilocarpine and refractory to midazolam, deep hypothermia (20. °C for 30. min) reduced EEG power over 50-fold, stopped SE within 12. min, and reduced EEG spikes by 87%. Hypothermia deserves further investigation as a treatment of last resort for refractory SE.This article is part of a Special Issue entitled "Status Epilepticus". © 2015 . Source

Torolira D.,Epilepsy Research Laboratory 151 | Suchomelova L.,Epilepsy Research Laboratory 151 | Wasterlain C.G.,Epilepsy Research Laboratory 151 | Wasterlain C.G.,University of California at Los Angeles | And 2 more authors.
Epilepsy Research | Year: 2016

Objective: Status Epilepticus (SE) is common in neonates and infants, and is associated with neuronal injury and adverse developmental outcomes. However, the role of SE in this injury is uncertain. Until now, we have lacked an animal model in which seizures result in neuronal injury in rodent models at ages below postnatal day 12 (P12) unless seizures are combined with inflammatory stressors. Methods: We induced SE with high-dose lithium and pilocarpine in P7 rats, which are developmentally close to human neonates. Several EEG measures and O2 saturation were recorded during the 6 h following initiation of SE. We assessed neuronal injury at 6 and 24 h post-SE onset using Fluoro-Jade B staining (FJB) and caspase-3a immunoreactivity (IR). Results: EEGs showed continuous polyspikes activity for 54.3 ± 6.7 min, while O2 saturation showed no significant hypoxemia. By 24 h after SE onset, significant neuronal injury was observed in CA1/subiculum, CA3, dentate gyrus, thalamus, neocortex, amygdala, piriform cortex, lateral entorhinal cortex, hypothalamus, caudate putamen, globus pallidus, ventral pallidum, and nucleus accumbens. At 24 h post-SE, caspase-3a IR was significantly increased in CA1/subiculum, thalamus, and neocortex compared to sham, and caspase-3a IR neurons had fragmented nuclei, suggesting that SE triggered an irreversible form of cell injury. Significance: In conclusion, we have developed a model of cholinergic SE in P7 rat pups, which combines high survival (69.9% survival at 24 h) and widespread brain injury. These studies suggest that the immature brain is vulnerable to severe forms of SE. © 2015 Published by Elsevier B.V. Source

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