Prenatal Protein Malnutrition Affects the Density of GABAergic Interneurons During Hippocampus Development in Rats.

BACKGROUND: Prenatal protein malnutrition disrupts the pattern of maturation and development of the hippocampus and its neuroanatomy and increases inhibition of the granular cell layer of the fascia dentata. If local gamma-aminobutyric acid inter-neurons are partly responsible for inhibition of the hippocampus, it is reasonable to assume that there may be an increase in the gamma-aminobutyric acid cell population of prenatal protein malnutrition rats. OBJECTIVE: This experimental study was conducted to ascertain the effects of prenatal protein malnutrition on the density of GABAergic interneurons at the cornus ammonis and fascia dentata in rats. METHODS: Animals were investigated under two nutritional conditions: (i) prenatal protein malnutrition group fed 6% protein, and (ii) well-nourished control group fed 25% protein. Using an antibody for gamma-aminobutyric acid, immunoreactive cells (GABAergic) were assessed in the rostral-caudal direction of the dorsal hippocampus at four levels. RESULTS: (i) In 30-day-old rats with prenatal malnutrition, the fascia dentata had an average of 27% more GABAergic cells than the control group; this higher amount was not detectable at 90 days. (ii) There was a significant 18% increase in GABAergic neurons at level 1 of the cornus ammonis at 90 days of age. CONCLUSIONS: There was an increase in the population of interneurons in the fascia dentata and cornus ammonis in prenatal protein malnutrition rats. We conclude that prenatal hypoprotein malnutrition produces changes at 30 days in the fascia dentata. Results suggest that prenatal malnutrition also produces a delay in the programmed chronology of gamma-aminobutyric acid interneurons. Finally, in cornus ammonis, at 90 days of age, prenatal protein malnutrition showed an increase only at level 1; this effect may be evidenced in the long term, despite postnatal rehabilitation.

[Carbamazepine produces changes in the auditory pathway of Wistar rats]. / Cambios que produce la carbamazepina en la vía auditiva de ratas Wistar.

BACKGROUND: Different results have been reported by various authors in studies regarding the impact of the (carbamazepine) CBZ on the auditory evoked responses. OBJECTIVE: To evaluate the changes in auditory pathway at different sound intensities with CBZ at doses 30 mg/kg, in latencies and interpeak-interval brainstem auditory evoked potentials (BAEPs) in Wistar rats. MATERIAL AND METHODS: Twenty adult male Wistar rats (body weight mean, 280-300 g) were used as subjects in this study. BAEPs elicited by stimulus of (30, 50 and 70 dB nHL) intensity and BAEP were obtained with and without CBZ treatment. RESULTS: Peak latencies of BAEPs, between groups were different, in the group with CBZ peak latencies were delaying, but we compared interpeak-intervals between groups and we found significative differences in III-V and I-V at 70 dB nHL intensity. CONCLUSIONS: Our results suggest that CBZ modifies BAEPs interpeak-intervals at 70 dB, and latencies since they were delayed. Alterations in the generators of the later waves of BAEPs underlie, AED produced changes in hearing sensitivity with a single no toxic doses. Probably CBZ causes changes in endolymphatic ion composition in the rat inner ear, provoking that latency of BAEPs were delaying, but this requires further studies.

Chronic exposure to toluene changes the sleep-wake pattern and brain monoamine content in rats.

Toluene, found in glues and cleaners, is among the inhalants most commonly abused by workers and young drug addicts. In this study, we examined the changes in sleep patterns and monoamine content induced by chronic toluene exposure. Rats were chronically exposed to toluene vapors beginning at 30 days of age for a duration of 30 days. Experiment I was performed in a control group (n=10) and a chronic toluene exposure group (n=10). Rats were implanted with bipolar stainless steel electrodes for electroencephalographic recording (EEG). In experiment II, conducted in two other groups (control and exposed to toluene, n=10 each), animals were sacrificed by decapitation prior to chromatographic analysis. We found that chronic toluene administration affected the organization of sleep patterns and monoamine content. Dopamine (DA) and noradrenaline (NA) increased in the midbrain and striatum. 3,4-dihydroxyphenylacetic acid (DOPAC) increased only in the striatum. Midbrain levels of serotonin (5-HT) increased in the pons and decreased in the hypothalamus and striatum. 5-hydroxyindoleacetic acid (5-HIAA) increased in the pons, midbrain and striatum and decreased in the hypothalamus. Chronic toluene exposure induced changes in the serotonergic and dopaminergic systems and increased SWS and PS deficits. We conclude that toluene exposure disrupts the sleep-wake cycle by affecting the monoaminergic response in cerebral areas related to sleep.

Effects of oxcarbazepine on monoamines content in hippocampus and head and body shakes and sleep patterns in kainic acid-treated rats.

The aim of this work was to analyze the effect of oxcarbazepine (OXC) on sleep patterns, "head and body shakes" and monoamine neurotransmitters level in a model of kainic-induced seizures. Adult Wistar rats were administered kainic acid (KA), OXC or OXC + KA. A polysomnographic study showed that KA induced animals to stay awake for the whole initial 10 h. OXC administration 30 min prior to KA diminished the effect of KA on the sleep parameters. As a measure of the effects of the drug treatments on behavior, head and body shakes were visually recorded for 4 h after administration of KA, OXC + KA or saline. The presence of OXC diminished the shakes frequency. 4 h after drug application, the hippocampus was dissected out, and the content of monoamines was analyzed. The presence of OXC still more increased serotonin, 5-hidroxyindole acetic acid, dopamine, and homovanilic acid, induced by KA.