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