| Background Disorders of cortical development (DCDs) resulting from aberrant brain development are often associated with several forms of epilepsy and characteristic of medically intractable epilepsy. Although the morphological properties of neurons within these malformations are well understood, very little is known about the function of these neurons. In rats, prenatal carmustine (BCNU) exposure produces loss of lamination in cortical structures and distinct nodular heterotopia, which are prone to hyperexcitability of neurons and may contribute to the increased seizure susceptibility observed in these animals. To study the electrophysiology of dysplastic cortex, we developed an experimental model of DCDs by BCNU-exposure and investigated the changes in properties of voltage-dependent sodium current and high voltage-activated (HVA) calcium current and their epileptogenic mechanisms.Methods 1. The animal models of DCDs were established by BCNU-exposure in uterus. Six pregnant Sprague-Dawley rats were injected intraperitoneally with 20mg/kg of BCNU on embryonic day 15(E15), their pups were enrolled in model group. Another six were injected with a corresponding volume of 5% dextrose in water on E15, their offspring were taken as control. 2. Histological changes of cerebral cortex and hippocampus were detected by cresyl violet staining. 3. Daily activities of rats were observed. 4. EEG recordings were carried on P40. 5.Rats were induced seizures by Lithium Chloride-Pilocarpine intraperitoneal injection with a lower dose than routine. The latency and duration of seizure onset and mortality of two groups were compared. 6.Voltage-dependent sodium currents and HVA calcium currents were recording in acutely isolated CA1 pyramidal neurons using the whole-cell patch-clamp technique. We analyzed their properties and compared with...
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