Prenatal exposure to electroconvulsive seizures and phenytoin: development of benzodiazepine binding sites, reflex behaviors and seizure thresholds in exposed offspring.
Electroconvulsive seizures administered during the period of fetal benzodiazepine (BZ) binding site proliferation (days 16, 18 and 20 in gestation) significantly decreased the density of cerebral cortical benzodiazepine binding sites in exposed pups up to 21 days postnatal age. Significant decreases in seizure threshold were also found in exposed offspring. However, decreases in BZ sites were not accompanied by significant alterations in RO5-4864-displaceable benzodiazepine binding as seen after in utero exposure to phenytoin (DPH). Neither prenatal treatment affected the ability of GABA to enhance BZ binding in vitro. Prenatal exposure to electroshock delayed the onset of acoustic startle and eye-opening during postnatal development; similar effects were not seen following in utero exposure to DPH. These data suggest that prenatal exposure to seizures and DPH decrease postnatal BZ site proliferation by different mechanisms.
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D001921:Brain / Q000378:metabolism; D004597:Electroshock; D005260:Female; D005333:Fetus / Q000187:drug effects*; D010672:Phenytoin / Q000494:pharmacology*; D011247:Pregnancy; D051381:Rats; D011956:Receptors, Cell Surface / Q000032:analysis* / Q000187:drug effects; D011963:Receptors, GABA-A; D012018:Reflex / Q000502:physiology*; D012640:Seizures / Q000503:physiopathology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D011956:Receptors, Cell Surface; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; D010672:Phenytoin