Marciani M G, Santone G, Sancesario G, Massa R, Stanzione P, Bernardi G
Clinica Neurologica, Dipartimento di Sanità Pubblica, II Università di Roma-Tor Vergata, Italy.
Neurosci Lett. 1991 Aug 19;129(2):306-10. doi: 10.1016/0304-3940(91)90487-e.
A 10-min bilateral carotid occlusion (BCO) in Mongolian gerbils induces transient generalized epileptic discharges in the hippocampal and cortical regions, which are followed by long lasting interictal spiking activity. An initial peak of this activity occurs within 18-36 h after BCO, then it decreases slowly and completely disappears by the 6th-7th day. On the 7th day, morphological evidence shows a selective loss of CA1 hippocampal neurons. 4-(3-Phosphonopropyl)-2-piperazine-carboxylic acid (CPP), a competitive antagonist of the N-methyl-D-aspartate (NMDA) receptor was administered (7 or 15 mg/kg i.p.) immediately after clamping, and again every 12 h for 3 consecutive days. It induced a dose-related depression of epileptic activity, while, on the other hand, at both dosages, it always prevented the loss of CA1 neurons. The results are discussed in view of the different mechanisms mediating cell damage and epileptic activity.
对蒙古沙鼠进行10分钟的双侧颈动脉闭塞（BCO），会在海马体和皮质区域诱发短暂的全身性癫痫放电，随后出现持续较长时间的发作间期棘波活动。这种活动的初始峰值出现在BCO后的18 - 36小时内，然后缓慢下降，并在第6 - 7天完全消失。在第7天，形态学证据显示海马体CA1区神经元出现选择性丢失。在夹闭后立即给予4-(3-膦酰基丙基)-2-哌嗪羧酸（CPP），一种N-甲基-D-天冬氨酸（NMDA）受体的竞争性拮抗剂（7或15毫克/千克腹腔注射），并连续3天每12小时给药一次。它引起了与剂量相关的癫痫活动抑制，而另一方面，在这两种剂量下，它总是能防止CA1神经元的丢失。鉴于介导细胞损伤和癫痫活动的不同机制，对这些结果进行了讨论。
