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Hyperexcitability of the Hippocampal CA1 and the Dentate Gyrus in Rats Subchronically Exposed to a Substitute for Chlorofluorocarbons, 1‐Bromopropane Vapor

Hyperexcitability of the Hippocampal CA1 and the Dentate Gyrus in Rats Subchronically Exposed to a Substitute for Chlorofluorocarbons, 1‐Bromopropane Vapor: Yukiko Fueta, et al. The First Department of Medical Technology, School of Health Sciences, University of Occupational and Environmental Health—To investigate the effects on the central nervous system of subchronic exposure to 1‐bromopropane (1‐BP), which is a substitute for chlorofluorocarbons, we measured the hippocampal excitability of 1‐BP‐treated rats electrophysiologically. Male Wistar rats were exposed to 1 ‐BP for 6‐h in a day in an exposure chamber (1,500 ppm) for 4 wk. After the 1‐, 3‐ and 4‐wk inhalation, field excitatory postsynaptic potentials (fEPSPs), population spikes (PSs), fEPSP/spike (E/S) curve, paired‐pulse profiles of fEPSP slopes and PS amplitudes recorded from CA1 pyramidal neurons, and dentate granule cells of the hippocampal slice obtained from the rats were analyzed. In 1 ‐BP treated rats, E/S potentiation and a lower subthreshold of PSs were observed in the dentate gyrus (DG) after the 3 and 4‐wk inhalation. Paired‐ pulse inhibition was reduced at 5‐50 ms in the CA1 and at 5‐20 ms in the DG after all of the inhalation. These changes were not associated with paired‐pulse inhibition of fEPSPs. In the DG, the paired‐pulse inhibition at the short interpulse intervals in rats exposed to 1‐BP was pronounced by an application of A type gamma aminobutyric acid (GABA) receptor agonist pentobarbital. Impaired paired‐pulse inhibition of granule cells at the short interpulse intervals was recovered after the application of N‐methyl‐D‐aspartate (NMDA) type glutamate receptor antagonist DL‐2‐amino‐5‐phosphonopentanoic acid. Convulsing rats observed after the 4‐wk inhalation exhibited multiple PSs in the DG, and their second component was abolished by an application of this antagonist. Inhalation of 1‐BP increased the neuronal excitability in the hippocampal CA1 and the DG. The hyperexcitability of the granule cells in the DG was at least due to an over‐activation of NMDA receptors.