RESUMEN
Many quantitative animal studies examining the possible relationship between hippocampal neuronal loss and the development of epilepsy have examined only the dorsal hippocampus. The ventral hippocampus, however, represents the more homologous structure to the anterior hippocampus in humans, which is the area associated with the maximal damage in patients with temporal lobe epilepsy. This study tested the hypothesis that the ventral hippocampus has greater neuronal injury than the dorsal hippocampus in an animal model of chemoconvulsant-status epilepticus at postnatal day 20. Status epilepticus was induced in postnatal day 20 Sprague-Dawley rat pups with the chemoconvulsant lithium-pilocarpine and brain tissue was examined with Fluoro-Jade B. Horizontal sections (n=7) favoring a visualization of the ventral hippocampus showed marked Fluoro-Jade B staining in CA1, CA3, and hilar region. Coronal sections favoring a visualization of the dorsal hippocampus did not consistently show as robust a staining pattern in these regions. In coronal sections where both the dorsal and ventral hippocampus could be viewed, greater staining was always seen in ventral versus dorsal hippocampus. Quantitative analysis of cell counts demonstrated a significant difference between ventral and dorsal hippocampus in CA1 and CA3, but not hilus. These results demonstrate that in ventral hippocampus, lithium pilocarpine-induced status epilepticus consistently results in hippocampal neuronal injury in postnatal day 20 rats. This study shows the importance of including the ventral hippocampus in any analysis of seizure-induced hippocampal neuronal injury, and raises concerns about the accuracy of studies quantifying hippocampal neuronal loss when only the dorsal hippocampus is examined.
Asunto(s)
Hipocampo/patología , Neuronas/patología , Estado Epiléptico/patología , Animales , Modelos Animales de Enfermedad , Agonistas Muscarínicos/toxicidad , Pilocarpina/toxicidad , Ratas , Ratas Sprague-Dawley , Estado Epiléptico/inducido químicamenteRESUMEN
Preclinical models of pediatric posttraumatic epilepsy (PTE) are lacking. We hypothesized that traumatic brain injury (TBI), induced by controlled cortical impact, in immature rats would cause electroencephalographic (EEG) epileptiform activity and behavioral seizures. TBI or sham craniotomy was performed on postnatal day 17. Using video-EEG monitoring 4-11 months post-TBI, most TBI rats (87.5%) showed EEG spiking and one had spontaneous, recurrent seizures. Controls showed neither EEG spikes nor electrographic/behavioral seizures. Late seizures were rare after TBI, but EEG spiking was common and may represent a surrogate for PTE.
Asunto(s)
Lesiones Encefálicas/fisiopatología , Corteza Cerebral/fisiopatología , Epilepsia Postraumática/fisiopatología , Hipocampo/patología , Animales , Modelos Animales de Enfermedad , Electroencefalografía , Tamaño de los Órganos , Ratas , Ratas Sprague-Dawley , Procesamiento de Señales Asistido por ComputadorRESUMEN
Electrographic status epilepticus (ESE) is a medical emergency consisting of repetitive seizures and may result in death or severe brain damage. Epilepsy can develop following ESE. The properties of ESE (e.g., duration and intensity) are variable, as are the effects of putative therapeutic treatments. Therefore a straightforward method to quantify different components of ESE would be beneficial for both researchers and clinicians. A frequency range close to the gamma band was selected for extraction of seizure-related activity from the EEG. This filtering strategy reduced motion artifacts and other noise sources in the electrophysiological recordings, thus increasing the signal-to-noise ratio of the EEG spike activity. EEG spiking was quantified using an energy operator and modeled by an eighth-order polynomial. In a benzodiazepine-resistant rat model of pilocarpine-induced ESE, the efficacy of various pharmaceutical agents at suppressing ESE was analyzed with this and other methods on data collected for < or =24 h after ESE induction. This approach allows for the objective, quantitative, and rapid assessment of the effects of both short- and long-lasting pharmacological manipulations on ESE and other forms of prolonged repetitive electrical activity.