Behavioral evaluation of adult rats exposed in utero to maternal epileptic seizures.

We investigated the effects of exposure to maternal convulsive seizures in utero on the behavior of offspring. An epilepsy model was induced in female rats by administration of pilocarpine. Seizure frequency was evaluated for 60 days. The rats were then allowed to mate, and seizure frequency during pregnancy was recorded and compared with prepregnancy frequency. After birth, placentas of mothers were submitted for histopathological analysis. The behavior of the offspring was evaluated 3 months after birth. There was a decline in seizure frequency even though the placentas from epileptic mothers showed areas of ischemic infarction indicative of fetal hypoxia. Offspring of epileptic mothers manifested deficits in motor coordination in the rotarod test and increased immobility in the open-field test. No changes in anxiety and depression-like behaviors were observed. These results suggest that "in utero" exposure to maternal seizures can produce motor deficits in adult life, perhaps as a result of fetal hypoxia.

The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis.

PURPOSE: As reported by several authors, angiotensin II (AngII) is a proinflammatory molecule that stimulates the release of inflammatory cytokines and activates nuclear factor kappaB (NFkappaB), being also associated with the increase of cellular oxidative stress. Its production depends on the activity of the angiotensin converting enzyme (ACE) that hydrolyzes the inactive precursor angiotensin I (AngI) into AngII. It has been suggested that AngII underlies the physiopathological mechanisms of several brain disorders such as stroke, bipolar disorder, schizophrenia, and disease. The aim of the present work was to localize and quantify AngII AT1 and AT2 receptors in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis (MTS) submitted to corticoamygdalohippocampectomy for seizure control. METHOD: Immunohistochemistry, Western blot, and real-time PCR techniques were employed to analyze the expression of these receptors. RESULTS: The results showed an upregulation of AngII AT1 receptor as well as its messenger ribonucleic acid (mRNA) expression in the cortex and hippocampus of patients with MTS. In addition, an increased immunoexpression of AngII AT2 receptors was found only in the hippocampus of these patients with no changes in its mRNA levels. DISCUSSION: These data show, for the first time, changes in components of renin-angiotensin system (RAS) that could be implicated in the physiopathology of MTS.