Marciani M G, Santone G, Sancesario G, Massa R, Stanzione P, Bernardi G
Department of Public Health, University of Rome Tor Vergata, Italy.
Funct Neurol. 1993 Mar-Apr;8(2):115-20.
A 10-min bilateral carotid occlusion (BCO) in a control group of Mongolian gerbils, induced a transient generalized epileptic activity both in the hippocampal and in the cortical regions, associated with motor manifestations. After recirculation, spiking activity persisted, reaching its maximum peak within 18-36 h and then slowly decreasing till its total disappearance on the 6th-7th day. On the 7th day, histological studies manifested a selective loss of CA1 hippocampal neurons. The treated gerbils (divided in 2 groups according to the dosage used) were administered clonazepam (CZP), a benzodiazepine receptor agonist, immediately after clamping and again every 24 h for the following three days at dosages of 0.05 and 0.1 mg/kg i.p., respectively. The drug inhibited epileptic activity in a dose-dependent manner, while it prevented CA1 neuronal loss at both doses. These results point to a possible derangement of the GABAergic system which probably in turn triggers an exaggerated excitation.
在一组蒙古沙鼠对照组中进行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活动，并伴有运动表现。再灌注后，尖峰活动持续存在，在18 - 36小时内达到最高峰，然后缓慢下降，直至在第6 - 7天完全消失。在第7天，组织学研究显示海马体CA1神经元有选择性丢失。将接受治疗的沙鼠（根据所用剂量分为2组）在夹闭后立即给予氯硝西泮（CZP，一种苯二氮䓬受体激动剂），并在接下来的三天里每天一次，分别以0.05和0.1毫克/千克的腹腔注射剂量给药。该药物以剂量依赖的方式抑制癫痫活动，同时在两种剂量下都能防止CA1神经元丢失。这些结果表明γ-氨基丁酸能系统可能发生紊乱，这可能进而引发过度兴奋。
