prenatal exposure to 1-bromopropane causes delayed adverse effects on hippocampal neuronal excitability in the ca1 subfield of rat offspring

Objectives: neurotoxicity of 1-bromopropane (1-bp) has been reported in occupational exposure, but whether the chemical exerts developmental neurotoxicity is unknown. we studied the effects of prenatal 1-bp exposure on neuronal excitability in rat offspring. methods: we exposed dams to 1-bp (700 ppm, 6 h a day for 20 days) and examined hippocampal slices obtained from the male offspring at 2, 5, 8, and 13 weeks of age. we measured the stimulation / response (s/r) relationship and paired-pulse ratios (pprs) of the population spike (ps) at the interpulse intervals (ipis) of 5 and 10 ms in the ca1 subfield. results: prenatal 1-bp exposure enhanced s/r relationships of ps at 2 weeks of age; however, the enhancement diminished at 5 weeks of age until it reached control levels. prenatal 1-bp exposure decreased pprs of ps at 2 weeks of age. after sexual maturation, however, the pprs of ps increased at 5-ms ipi in rats aged 8 and 13 weeks. conclusions: our findings indicate that prenatal 1-bp exposure in dams can cause delayed adverse effects on excitability of pyramidal cells in the hippocampal ca1 subfield of offspring.