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Toxicological Sciences 61, 321-330 (2001)
Copyright © 2001 by the Society of Toxicology

NEUROTOXICOLOGY

Developmental Exposure of Rats to a Reconstituted PCB Mixture or Aroclor 1254: Effects on Long-Term Potentiation and [3H]MK-801 Binding in Occipital Cortex and Hippocampus

L. Altmann*,{dagger},1, W. R. Mundy§, T. R. Ward§, A. Fastabend*,{ddagger} and H. Lilienthal*,{dagger}

* Medical Institute of Environmental Hygiene at the Heinrich-Heine-University, Duesseldorf, Germany; Departments of {dagger} Neurobehavioral Toxicology, and {ddagger} Analytic Chemistry, Auf'm Hennekamp 50, D-40225 Duesseldorf, Germany; and § Neurotoxicology Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711

The central nervous system is one of the target organs for polychlorinated biphenyls (PCBs). We measured the effects of maternal exposure of Long-Evans rats to a mixture of PCB congeners reconstituted according to the pattern found in human breast milk (reconstituted mixture, RM) on long-term potentiation (LTP) in two brain regions. Exposure of the dams via food started 50 days prior to mating and was terminated at birth. In the first experiment, adult male and female offspring were exposed maternally to 40 mg/kg of the RM or the commercial mixture Aroclor 1254 (A1254). LTP and paired-pulse inhibition were measured in slices of the visual cortex. In addition, the binding of [3H]MK-801 to the N-methyl-D-aspartate (NMDA) receptor-ion channel as well as the [3H]muscimol binding to the GABA-A receptor in membrane preparations from the occipital cortex and hippocampus were determined. LTP as well as [3H]MK-801 binding were significantly reduced in the cortex following PCB exposure, while [3H]MK-801 binding in the hippocampus was not affected. In a succeeding experiment, LTP was determined in cortical and hippocampal slices from rats at postnatal days 10 to 20, following exposure to 0, 5, or 40 mg/kg of the RM. Cortical LTP was significantly affected by the RM while no effects were seen in hippocampal LTP. Taking the two experiments together, PCB exposure significantly reduced LTP, as well as [3H]MK-801 binding, in the cortex and had no effect in the hippocampus. The LTP deficits can only partly be related to the reduction of binding sites to the NMDA receptor; other PCB-induced neurochemical changes have to be assumed.

Key Words: polychlorinated biphenyls; NMDA receptor; long-term potentiation; visual cortex; hippocampus; brain slices.


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