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Neonatal exposure to brominated flame retardant BDE-47 reduces long-term potentiation and postsynaptic protein levels
Milou M L Dingemans1, Geert M J Ramakers, Fabrizio Gardoni
1Toxicology Division, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands. M.Dingemans@iras.uu.nl
Insights
Neonatal exposure to brominated flame retardants like BDE-47 impairs synaptic plasticity in mice. This study reveals reduced long-term potentiation and altered postsynaptic proteins in the hippocampus, suggesting neurodevelopmental risks.
Area of Science:
- Neuroscience
- Environmental Toxicology
- Developmental Biology
Background:
- Environmental polybrominated diphenyl ethers (PBDEs) raise concerns due to potential adverse effects, especially following early developmental exposure.
- Previous research indicated behavioral impairments after neonatal PBDE exposure, necessitating investigation into underlying neurodevelopmental mechanisms.
Purpose of the Study:
- To investigate the neurodevelopmental mechanisms responsible for behavioral impairments observed after neonatal exposure to PBDEs.
- To examine the effects of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) on synaptic plasticity and associated molecular changes in the developing mouse brain.
Main Methods:
- Neonatal C57Bl/6 mice received a single oral dose of BDE-47 during the brain growth spurt (postnatal day 10).
- Ex vivo electrophysiological recordings (f-EPSP) assessed synaptic plasticity (LTP, paired-pulse facilitation) in the hippocampus.
- Western blotting analyzed levels of key postsynaptic proteins, including glutamate receptor subunits and CaMKII.
- In vitro studies using rat pheochromocytoma (PC12) cells investigated acute effects on catecholamine release and intracellular calcium.
Main Results:
- Exposure to BDE-47 significantly reduced long-term potentiation (LTP) in the hippocampal CA1 area.
- Western blot analysis revealed decreased levels of glutamate receptor subunits (NR2B, GluR1) and active Ca(2+)/calmodulin-dependent protein kinase II (alphaCaMKII) in the postsynaptic fraction.
- In vitro studies showed modest effects on vesicular release and intracellular calcium in PC12 cells, suggesting a predominantly postsynaptic mechanism in vivo.
Conclusions:
- Early neonatal exposure to a high dose of BDE-47 leads to reduced hippocampal LTP in mice.
- Observed changes in postsynaptic proteins involved in synaptic plasticity indicate a disruption of neuronal function.
- The findings suggest that PBDEs can interfere with critical neurodevelopmental processes, potentially leading to long-term consequences.
Background:
Increasing environmental levels of brominated flame retardants raise concern about possible adverse effects, particularly through early developmental exposure.
Objective:
The objective of this research was to investigate neurodevelopmental mechanisms underlying previously observed behavioral impairments observed after neonatal exposure to polybrominated diphenyl ethers (PBDEs).
Methods:
C57Bl/6 mice received a single oral dose of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) on postnatal day (PND) 10 (i.e., during the brain growth spurt). On PND17-19, effects on synaptic plasticity, levels of postsynaptic proteins involved in long-term potentiation (LTP), and vesicular release mechanisms were studied ex vivo. We investigated possible acute in vitro effects of BDE-47 on vesicular catecholamine release and intracellular Ca(2+) in rat pheochromocytoma (PC12) cells.
Results:
Field-excitatory postsynaptic potential (f-EPSP) recordings in the hippocampal CA1 area demonstrated reduced LTP after exposure to 6.8 mg (14 micromol)/kg body weight (bw) BDE-47, whereas paired-pulse facilitation was not affected. Western blotting of proteins in the postsynaptic, triton-insoluble fraction of hippocampal tissue revealed a reduction of glutamate receptor subunits NR2B and GluR1 and autophosphorylated-active Ca(2+)/calmodulin-dependent protein kinase II (alphaCaMKII), whereas other proteins tested appeared unaffected. Amperometric recordings in chromaffin cells from mice exposed to 68 mg (140 micromol)/kg bw BDE-47 did not reveal changes in catecholamine release parameters. Modest effects on vesicular release and intracellular Ca(2+) in PC12 cells were seen following acute exposure to 20 microM BDE-47. The combined results suggest a post-synaptic mechanism in vivo.
Conclusion:
Early neonatal exposure to a single high dose of BDE-47 causes a reduction of LTP together with changes in postsynaptic proteins involved in synaptic plasticity in the mouse hippocampus.
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