Abstract
1-Bromopropane (CH3CH2CH2Br 1-BP) is a newly introduced substitute for specific chlorofluorocarbons whose production was prohibited because of depletion of ozone layers, and is mainly used for degreasing agents and spray adhesives. Although case studies in the USA and China have demonstrated that 1-BP could adversely affect the human nervous system, the underlying mechanism for the effects of 1-BP inhalation exposure on the CNS has not been understood. We investigated the effects of 1-BP exposure on the CNS using different models of exposure. 1-BP potentiated GABA but inhibited ACh responses in Xenopus oocytes expressing GABAA and nicotinic ACh receptors, respectively, and enhanced recurrent inhibition in the rat hippocampus. On the other hand, hippocampal disinhibition was observed in a concentration-dependent manner (200–1500 ppm) after chronic inhalation of 1-BP in the rats and, at the highest concentration of 1-BP inhalation, epileptic potentials were evoked in the dentate gyrus. Moreover, prenatal exposure to 1-BP vapor resulted in enhanced stimulation/response (S/R) curve of population spikes in the CA1 area of PND 11-15 rats and reduced S/R curve of field excitatory postsynaptic potentials in the CA1 area in adults (6-8w). These results suggest that 1-BP inhalation exposure disrupts neuronal excitability of the hippocampal formation. [J Physiol Sci. 2006;56 Suppl:S22]
