Epileptic Rat Brain Research Articles

Glucose utilization during interictal intervals in an epilepsy model induced by pilocarpine: a qualitative study.

Interictal intervals in pilocarpine-induced chronic epilepsy are characterized by apparent normal electrographic activity and longer sleep periods or drowsiness or both. Sparse information exists concerning the neural network activity during these seizure-free intervals. In our research, a [14C]2-deoxy-D-glucose (2DG) autoradiographic technique was used to investigate interictal changes in the metabolism of the epileptic rat brain. Epileptic rats were monitored by video-EEG for approximately 120 days, with [14C]2DG injected after a seizure-free interval of > or = 24 h. Autoradiographic analysis revealed an increase in glucose utilization by several brain regions; the most consistent increase was found in the lateral posterior thalamic nucleus and pretectal region. These findings suggest that the lateral posterior thalamic nucleus and the pretectal region may be involved in cerebral circuits inhibiting epileptic activity during interictal intervals.

Postictal alteration of sodium content and apparent diffusion coefficient in epileptic rat brain induced by kainic acid.

We studied temporal changes of brain sodium and apparent diffusion coefficient (ADC) in a temporal lobe epilepsy (TLE) rat model using kainic acid (KA). In situ three-dimensional 23Na magnetic resonance imaging (MRI) and proton diffusion-weighted imaging (DWI) were used. KA at a dose of 10 mg/kg body weight and 12 adult Sprague Dawley rats weighing 228-318 g (268 +/- 25 g) were used. Twenty-four hours after KA injection, magnetic resonance (MR) visible sodium levels increased in both the pyriform cortex (+90%) and amygdala (+68%) and increased insignificantly in the hippocampus (+18%) and caudate-putamen (12%). The ADC in the pyriform cortex showed a -9% decrease at 5 h postictally, reaching -30% at 24 h, whereas in the amygdala decreases were -8 and -26% respectively. A significant decrease in ADC (-7%) in the hippocampus was also observed 24 h postically. Seven days later, sodium increases persisted, whereas ADC returned to normal level. The increase in MR visible sodium, associated with the decrease in ADC is consistent with the hypothesis that sequential seizures caused an increase in sodium influx and perturbation of membrane ion homeostasis, which eventually evolved into an irreversible phase of cellular edema, with increased MR visible intracellular sodium and decreased ADC. Return of ADC to near-control level and persistent high sodium level at 7 days may be explained by the increase in extracellular space and tissue necrosis.

Elevated concentration of glycogen in cobalt induced epileptogenic focus

Changes in the concentration of glycogen in various areas of the brain of epileptic rats were investigated. Epilepsy was induced by implantation of cobalt discs on the right sensory motor cortex and epileptic animals have shown clear tonic-clonic jerks of the contra-lateral fore and hind limbs. It was found that glycogen concentration was increased by 29% in the epileptogenic sensory motor cortex as compared to the same area in the contra-lateral hemisphere. Glycogen concentration in other areas within the same hemisphere remained unaffected. Implantation of nickel or copper on the same sensory motor cortex, which did not cause the typical limb jerks of epilepsy, had no effect on glycogen concentration in the same treated areas. Assay of relevant metabolites in the epileptic cortex showed an increase in the concentration of pyruvate and glucose-6-phosphate, by 218% and 112% respectively. The results suggest that the increased glycogen concentration in epileptogenic focus results from increased uptake of glucose due to neuronal hyperexcitability.

Epilepsy and hormonal regulation: the patterns of GnRH and galanin immunoreactivity in the hypothalamus of epileptic female rats

Endocrine and reproductive alterations are frequently reported to occur in women with temporal lobe epilepsy as well as in female rats in different experimental models of limbic seizures. We have recently observed that rats with structural damage of limbic structures induced by sustained convulsions triggered by systemic administration of pilocarpine develop spontaneous seizures after a mean latency of 15 days. In order to investigate the possible substrate of endocrine alterations in epilepsy, changes of the gonadotropin-releasing hormone (GnRH) and the neuropeptide galanin (GAL) were studied in the hypothalamus of epileptic female rats after pilocarpine treatment. Female rats injected with pilocarpine (320–350 mg/kg, i.p.) and control cases injected with saline were killed 10–20 h, 10–15 or 60–90 days following treatment. In some of these animals colchicine was injected in the lateral cerebral ventricle 24 h before death. GnRH immunopositivity was observed in the hypothalamus in neuronal cell bodies, fibers and punctate elements of both epileptic and control cases. A striking reduction of the density of GnRH-immunoreactive fibers and puncta was observed in the hypothalamus of the epileptic female rats killed 10–15 or 60–90 days following pilocarpine administration. No significant differences were observed in the number and size of GAL-immunoreactive perikarya of epileptic and control cases. The present findings suggest that a substantial rearrangement of GnRH-containing efferents, and in particular a loss of their terminal branches, occurs in the epileptic rat brain. Comparable regressive changes could account for alterations in endocrine and reproductive functions observed in temporal lobe epilepsy.