Developmental exposure to a commercial PCB mixture (Aroclor 1254) produces a persistent impairment in long-term potentiation in the rat dentate gyrus in vivo1The information in this document has been funded by the US Environmental Protection Agency. It has been subjected to review by the National Health and Environmental Effects Research Laboratory and approved for publication. Approval does not signify that the contents reflect the views of the Agency, nor does mention of trade names or commercial products constitute endorsement or recommendation for use.1

These receptor- and hormone-dependent disturbances are functionally reflected in electrophysiological deficits, including reduced hippocampal and dentate gyrus LTP after developmental exposure to Aroclor 1254 or CB-77.

“These receptor- and hormone-dependent disturbances are functionally reflected in electrophysiological deficits, including reduced hippocampal and dentate gyrus LTP after developmental exposure to Aroclor 1254 or CB-77 (Gilbert and Crofton, 1999; Ogiue-Ikeda et al., 2008; Zoeller et al., 2000).”

PAHs converge on related mechanisms through AhR activation; BaP reduces glutamate concentration and glutamate receptor expression, thereby weakening hippocampal LTP and impairing learning and memory; anthracene disrupts cholinergic signaling through acetylcholinesterase inhibition, leading to prolonged presence of acetylcholine in the synaptic cleft.

“PAHs converge on related mechanisms through AhR activation; BaP, for example, reduces glutamate concentration and glutamate receptor expression, thereby weakening hippocampal LTP and impairing learning and memory, while anthracene further disrupts cholinergic signaling through acetylcholinesterase inhibition which leads to the prolonged presence of acetylcholine in the synaptic cleft (Brown et al.”

Coplanar PCB congeners such as CB-77 and dioxins such as TCDD bind AhR with high affinity, leading to dysregulated gene expression and increased neuronal apoptosis.

“Coplanar PCB congeners such as CB-77 and dioxins such as TCDD bind AhR with high affinity, leading to dysregulated gene expression and increased neuronal apoptosis (Gilbert and Crofton, 1999; Parent et al., 2011).”