Gilbert M E, Liang D
National Research Council, Neurotoxicology Division, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA.
Neurotoxicol Teratol. 1998 Jul-Aug;20(4):383-9. doi: 10.1016/s0892-0362(98)00005-1.
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.
发育期接触多氯联苯（PCBs）与包括认知功能障碍在内的多种神经学效应有关。本研究评估了急性体外暴露于高氯代PCBs的复杂混合物——艾氏剂1254（A1254）对大鼠海马体突触传递的影响。在从CA1锥体细胞层记录的场电位中，观察到响应1.0 - 3微克/毫升的A1254时群体峰电位（PS）幅度增加。在开始暴露于3微克/毫升A1254后5 - 10分钟，PS幅度增加了约20%，尽管持续灌注，但到30分钟时部分恢复到基线幅度。更长时间的暴露显示，在暴露于3微克/毫升A1254超过90分钟后，PS幅度持续维持10%的增加。辐射层中的第二个记录电极显示兴奋性突触后电位（EPSP）斜率适度增加（约10%），且是短暂的。EPSP斜率变化在暴露于A1254（3微克/毫升）后5分钟内出现，在10分钟时达到峰值，尽管继续用A1254灌注，但到30分钟时降至基线水平。长期监测显示，回到基线水平后EPSP斜率幅度相对稳定。长时程增强（LTP）是一种突触可塑性模型，被认为包含记忆的生理基础。从锥体层记录的PS增强的幅度和持续性均不受3微克/毫升A1254的影响。在辐射层记录的EPSP斜率的LTP在对照切片和A1254处理的切片中也被诱导到相当程度。然而，在训练后60分钟的记录期内，处理切片中树突反应的增强并未维持。PCBs对钙稳态、蛋白激酶C易位、多巴胺能功能和激素作用的急性影响可能导致了在海马体突触传递和可塑性中所见的效应模式。
