Horn E, Esseling K
Abteilung für Neurologie, Universitätsklinikum Ulm, Germany.
Pharmacol Biochem Behav. 1993 Aug;45(4):857-63. doi: 10.1016/0091-3057(93)90132-d.
Experiments were performed to answer the question, whether series of generalized tonic-clonic seizures, induced in the awake rat by a local injection of Na-penicillin (PCN) solution into the motor cortex, terminates at the same critical concentration Ct of PCN within the focal area independently of the concentration C0 of PCN injected. Using the PCN diffusion coefficient D = 3.52 x 10(-4) mm2/s and the tortuosity factor lambda = 1.62, the concentration Ct at the onset of the last generalized seizure was calculated. The median duration of seizure series increased from 32 to 190 min, when the dose of injected PCN was raised from 32 to 1000 IU. At the onset of the last seizure, the median concentration Ct within the artificial focus ranged from 2.1 to 4.0 IU/0.5 microliter saline in rats treated with 32 to 125 IU PCN. After induction of convulsive behaviour with C0 = 250, 500, or 1000 IU PCN/0.5 microliter saline, however, Ct was at a higher level between 6.1 and 7.4 IU PCN/0.5 microliter saline. The difference between the cumulated data from the low-dose vs. the high-dose range was significant (p < 0.01). It is concluded that during long-lasting series of generalized seizures, the brain takes advantage of its plastic properties. By forming a counteracting mechanism, it protects itself from extreme epileptiform activity. This autoprotection may be due to the activation of neuronal networks which probably needs a certain frequency of seizures to become operatively.
通过将青霉素钠(PCN)溶液局部注射到清醒大鼠的运动皮层所诱发的一系列全身性强直阵挛性发作,是否会在局灶区域内PCN的相同临界浓度Ct处终止,而与所注射PCN的浓度C0无关。利用PCN扩散系数D = 3.52×10⁻⁴mm²/s和曲折因子λ = 1.62,计算了最后一次全身性发作开始时的浓度Ct。当注射的PCN剂量从32 IU增加到1000 IU时,发作系列的中位持续时间从32分钟增加到190分钟。在用32至125 IU PCN治疗的大鼠中,在最后一次发作开始时,人工病灶内的中位浓度Ct在2.1至4.0 IU/0.5微升盐水中。然而,在用C0 = 250、500或1000 IU PCN/0.5微升盐水诱发惊厥行为后,Ct处于6.1至7.4 IU PCN/0.5微升盐水的较高水平。低剂量与高剂量范围的累积数据之间的差异具有统计学意义(p < 0.01)。结论是,在长期的全身性癫痫发作系列中,大脑利用其可塑性。通过形成一种对抗机制,它保护自己免受极端癫痫样活动的影响。这种自我保护可能是由于神经元网络的激活,而这可能需要一定频率的癫痫发作才能发挥作用。