Swartzwelder H S, Wilson W A
Epilepsia. 1987 May-Jun;28(3):207-13. doi: 10.1111/j.1528-1157.1987.tb04209.x.
Stimulus train-induced bursting (STIB) in the hippocampal slice is an in vitro model of epileptiform activity that is analogous to kindling and requires no manipulation of the neurochemical or ionic environment. The bursts recorded from slices after STIB closely resemble the discharges observed in vivo after kindling and may provide a convenient and accessible model for studies of the electrophysiological underpinnings of epileptiform bursting in local neural circuits. One critical element in the validation of this model is the responsiveness of STIB to traditional sedatives and anticonvulsants. In this study we assessed the effects of the barbiturates phenobarbital and pentobarbital on both spontaneous and stimulus-triggered bursts after STIB. Concentration-response studies indicated that both drugs had inhibitory effects on stimulus-triggered bursting, although at significantly different concentrations. The rate of spontaneous bursting, however, was not significantly affected by phenobarbital at any of the concentrations tested, whereas pentobarbital reduced the frequency of spontaneous bursting in a concentration-dependent manner. These results indicate that STIB is responsive to the barbiturates tested, although the drugs have differential potencies depending on the type of bursting measured. These effects may be the result of differential potencies of these drugs on gamma-aminobutyric acid-mediated inhibition within local hippocampal circuits, as well as different effects on the biophysical characteristics of pacemaker cells within these circuits.
海马切片中的刺激串诱导爆发(STIB)是一种癫痫样活动的体外模型,类似于点燃模型,且无需对神经化学或离子环境进行操作。STIB后从切片记录的爆发与点燃后在体内观察到的放电非常相似,可能为研究局部神经回路中癫痫样爆发的电生理基础提供一个方便且易于使用的模型。该模型验证的一个关键要素是STIB对传统镇静剂和抗惊厥药的反应性。在本研究中,我们评估了巴比妥类药物苯巴比妥和戊巴比妥对STIB后自发和刺激触发爆发的影响。浓度-反应研究表明,两种药物对刺激触发的爆发均有抑制作用,尽管所需浓度显著不同。然而,在所测试的任何浓度下,苯巴比妥对自发爆发率均无显著影响,而戊巴比妥则以浓度依赖的方式降低自发爆发的频率。这些结果表明,STIB对所测试的巴比妥类药物有反应,尽管根据所测量的爆发类型,药物的效力有所不同。这些效应可能是由于这些药物对局部海马回路中γ-氨基丁酸介导的抑制作用的效力不同,以及对这些回路中起搏器细胞生物物理特性的不同影响所致。