Prenatal exposure to 1-bromopropane causes delayed adverse effects on hippocampal neuronal excitability in the CA1 subfield of rat offspring

J Occup Health. 2018 Jan 25;60(1):74-79. doi: 10.1539/joh.17-0009-BR. Epub 2017 Nov 1.

Abstract

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.

Keywords: 1-Bromopropane; Delayed adverse effect; Electrophysiology; Excitability; Prenatal exposure; Rat hippocampal slices.

MeSH terms

  • Animals
  • CA1 Region, Hippocampal / drug effects*
  • Cortical Excitability / drug effects*
  • Female
  • Hydrocarbons, Brominated / toxicity
  • Male
  • Neurotoxicity Syndromes / etiology
  • Neurotoxicity Syndromes / physiopathology*
  • Pregnancy
  • Prenatal Exposure Delayed Effects / chemically induced
  • Prenatal Exposure Delayed Effects / physiopathology*
  • Rats
  • Rats, Wistar

Substances

  • Hydrocarbons, Brominated
  • 1-bromopropane