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Methyl bromide decreases excitability without having immediate toxic effects in rat hippocampal CA1 neurons in vitro
M L Zeise1, D Jofré, P Morales
1University of Santiago de Chile, Technological Faculty, Program of Management in Agriculture. mzeise@lauca.usach.cl
Abstract:
Methyl bromide, a disinfectant gas amply used worldwide, is neurotoxic in humans and other mammals. To study its short-term effects on neurons, it was applied in aqueous solution to hippocampal slices of young rats (1.4 and 0.7 mM; for 8 minutes). Extracellular field recordings and intracellular microelectrode recordings from CA1 pyramidal neurons showed that the neurons stay viable for at least one hour after application of the mono-halomethane. However, a moderate, but consistent, irreversible decrease in synaptic excitability was observed. The intracellular recordings indicate that this may be attributed to a decrease in excitatory postsynaptic potentials. No effects were observed at 0.7 mM methyl bromide. Bromide, in a dose-dependent, partly reversible manner (during one hour), produced a similar decrease in excitability. Quantitatively, the action of bromide at 0.5 mM resembled the one seen with methyl bromide at the concentration of 1.4 mM. Since methyl bromide did not induce electrophysiologic changes consistent with evidence of neurotoxicity during one hour of observation it is concluded that it lacks immediate toxic effects on hippocampal rat neurons. Its neurotoxicity may be entirely due to metabolites or other indirect effects. The slight decrease in excitability may be due to the effect of bromide that is set free as tissue proteins and other cell molecules are methylated.
Insights
Methyl bromide, a neurotoxic disinfectant, did not show immediate toxic effects on rat hippocampal neurons. Its observed effects on synaptic excitability were attributed to bromide, not direct neurotoxicity.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Methyl bromide is a widely used disinfectant with known neurotoxicity in mammals.
- Understanding its short-term effects on neuronal function is crucial for risk assessment.
Purpose of the Study:
- To investigate the immediate electrophysiological effects of methyl bromide on rat hippocampal neurons.
- To differentiate between direct neurotoxicity and indirect effects, such as those from bromide.
Main Methods:
- Application of methyl bromide (1.4 and 0.7 mM) to rat hippocampal slices.
- Extracellular field and intracellular microelectrode recordings from CA1 pyramidal neurons.
- Comparison with the effects of bromide application.
Main Results:
- Neurons remained viable for at least one hour post-application.
- A moderate, irreversible decrease in synaptic excitability was observed at 1.4 mM methyl bromide, linked to reduced excitatory postsynaptic potentials.
- No effects were seen at 0.7 mM methyl bromide.
- Bromide induced a dose-dependent, partly reversible decrease in excitability, quantitatively similar to methyl bromide's effect.
Conclusions:
- Methyl bromide lacks immediate electrophysiological toxic effects on hippocampal neurons within one hour.
- Observed excitability changes are likely due to released bromide, not direct neurotoxicity.
- The neurotoxicity of methyl bromide may stem from metabolites or indirect mechanisms.