Prenatal Exposure to 1-Bromopropane Suppresses Kainate-Induced Wet Dog Shakes in Immature Rats.

1-Bromopropane (1-BP) is used in degreasing solvents and spray adhesives. The adverse effects of 1-BP have been reported in human cases and adult animal models, and its developmental toxicity has also been reported, but its effects on developmental neurotoxicity have not been investigated in detail. We evaluated the effects in rat pups of prenatal exposure to 1-BP on behaviors such as scratching and wet dog shakes (WDS), which were induced by injection of kainate (KA). Pregnant Wistar rats were exposed to vaporized 1-BP with 700 ppm from gestation day 1 to day 20 (6 h/day). KA at doses of 0.1, 0.5, and 2.0 mg/kg were intraperitoneally injected into a control group and a 1-BP-exposed group of pups on postnatal day 14. There was no significant difference in scratching between the control and the prenatally 1-BP-exposed groups, while suppression of the occurrence ratio of WDS was observed at the low dose of 0.1 mg/kg of KA in the prenatally 1-BP-exposed pups. Our results suggest that prenatal exposure to 1-BP affects neurobehavioral responses in the juvenile period.

Development of a direct exposure system for studying the mechanisms of central neurotoxicity caused by volatile organic compounds.

Many volatile organic compounds (VOCs) used in work places are neurotoxic. However, it has been difficult to study the cellular mechanisms induced by a direct exposure to neurons because of their high volatility. The objective of this study was to establish a stable system for exposing brain slices to VOCs. With a conventional recording system for brain slices, it is not possible to keep a constant bath concentration of relatively highly volatile solvents, e.g. 1-bromopropane (1-BP). Here we report a new exposure system for VOCs that we developed in which a high concentration of oxygen is dissolved to a perfused medium applying a gas-liquid equilibrium, and in which the tubing is made of Teflon, non adsorptive material. Using our system, the bath concentration of the perfused 1-BP remained stable for at least 2 h in the slice chamber. Both 6.4 and 2.2 mM of 1-BP did not change the paired-pulse response, but fully suppressed long-term potentiation in the dentate gyrus (DG) of hippocampal slices obtained from rats, suggesting that 1-BP decreases synaptic plasticity in the DG at the concentrations tested. Our new system can be applicable for investigating the underlying mechanisms of the neurotoxicity of VOCs at the cellular level.