Developmental exposure to a commercial PCB mixture (Aroclor 1254) producesa persistent impairment in long-term potentiation in the rat dentate gyrusin vivo

Citation
Me. Gilbert et Km. Crofton, Developmental exposure to a commercial PCB mixture (Aroclor 1254) producesa persistent impairment in long-term potentiation in the rat dentate gyrusin vivo, BRAIN RES, 850(1-2), 1999, pp. 87-95
Citations number
89
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BRAIN RESEARCH
ISSN journal
00068993 → ACNP
Volume
850
Issue
1-2
Year of publication
1999
Pages
87 - 95
Database
ISI
SICI code
0006-8993(199912)850:1-2<87:DETACP>2.0.ZU;2-A
Abstract
Developmental exposure to polycholorinated biphenyls (PCBs) has been associ ated with cognitive deficits in humans and laboratory animals. The present study sought to examine synaptic plasticity in the hippocampus, a brain reg ion critical for some types of memory function, in animals exposed to PCBs early in development. Pregnant Long-Evans rats were administered either cor n oil (control) or 6 mg/kg/day of a commercial PCB mixture, Aroclor 1254 (A 1254) by gavage from gestational day (GD) 6 until pups were weaned on postn atal day (PND) 21. In adult male offspring (3-6 months of age), field poten tials evoked by perforant path stimulation were recorded in the dentate gyr us under urethane anesthesia. Input/output (I/O) functions were assessed by averaging the response evoked in the dentate gyrus to stimulus pulses deli vered to the perforant path in an ascending intensity series. Long-term pot entiation (LTP) was induced by delivering a series of brief high frequency (400 Hz) train bursts to the perforant path at a moderate stimulus intensit y and I/O functions were reassessed 1 h later. No differences in baseline s ynaptic population spike (PS) and minor effects on excitatory postsynaptic potential (EPSP) slope amplitudes were discerned between the groups prior t o train delivery. Post-train I/O functions, however, revealed a 50% decreme nt in the magnitude of LTP in PCB-exposed animals. These data are the first to demonstrate persistent decrements in hippocampal synaptic plasticity in the intact animal following developmental exposure to PCBs. Disruption of early brain ontogeny due to developmental PCB exposure may underlie perturb ations in the neurological substrates that support synaptic plasticity and contribute to deficits in LTP and learning that persist into adulthood. (C) 1999 Published by Elsevier Science B.V. All rights reserved.