Abstract

Developmental exposure to polychlorinated biphenyls (PCBs) has been associated with a variety of neurological effects including cognitive dysfunction. The present study assessed the effects of acute in vitro exposure to a complex mixture of highly chlorinated PCBs, Aroclor 1254 (A1254), on synaptic transmission in the hippocampus of the rat. Increases in population spike (PS) amplitude were observed in field potentials recorded from the pyramidal cell layer of CA1 in response to 1.0-3 microg/ml of A1254. PS amplitude was increased by approximately 20% 5-10 min following the beginning of exposure to 3 microg/ml A1254, with some recovery towards baseline amplitudes occurring by 30 min, despite continuous perfusion. Longer exposures revealed that a maintained 10% increase in PS amplitude persisted beyond 90 min of exposure to 3 microg/ml A1254. A second recording electrode in the stratum radiatum revealed modest increases in EPSP slope (approximately 10%) that were transient. EPSP slope changes appeared within 5 min of exposure to A1254 (3 microg/ml), peaked at 10 min, and declined to baseline levels by 30 min, despite continued perfusion with A1254. Monitoring over a protracted period revealed relatively stable EPSP slope amplitudes following the return to baseline levels. Long-term potentiation (LTP) is a model of synaptic plasticity believed to encompass the physiological substrates of memory. Neither magnitude or persistence of PS potentiation recorded from the stratum pyramidale was affected by 3 microg/ml A1254. LTP of the EPSP slope recorded in the stratum radiatum was also induced to a comparable degree in control and A1254-treated slices. However, the augmentation in the dendritic response was not maintained in the treated slices over the 60-min posttrain recording period. Acute effects of PCBs on calcium homeostasis, protein kinase C translocation, dopaminergic function, and hormonal action may contribute to the pattern of effects seen in synaptic transmission and plasticity in the hippocampus.

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