Abstract
We produced limbic status epilepticus in rats by injecting a combination of dibutyryl-cAMP (db-cAMP) and ethylenediaminetetraacetic acid (EDTA) into the amygdala (AM). Thirty minutes after intra-AM db-cAMP/EDTA injection, thyrotropin-releasing hormone (TRH) was administered intravenously or intracerebroventricularly. Intravenous TRH (3, 25, 50 mg/kg) produced immediate activation of electroclinical seizures, lasting for 25–45 min. In some animals which showed this seizure activation, complete seizure suppression occurred 55–70 min after the TRH treatment. Similar activation of ictal seizures with delayed seizure suppression was obtained after intracerebroventricular TRH (25, 50 μg). The findings suggest that the effects of intravenous TRH are due to its central action and that the use of intravenous TRH is not a promising approach for the treatment of status epilepticus.
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