Tortosa A, Ferrer I
Unidad de Neuropatologia, Hospital Príncipes de Espaãna, Universidad de Barcelona, Spain.
Neuroscience. 1993 Jul;55(1):33-43. doi: 10.1016/0306-4522(93)90452-l.
Parvalbumin immunoreactivity is examined in the hippocampus of the Mongolian gerbil (Meriones unguiculatus) in controls and in animals subjected to 20 min of forebrain ischaemia produced by bilateral clipping of the carotids. In comparison with other species, the hippocampus of the gerbil is characterized by strong immunoreactivity of the (presumably excitatory) perforant pathway, and weak immunoreactivity (low numbers of neurons and scarce dendritic arbors) in nonpyramidal nerve cells (inhibitory neurons) of the CA1 area. These properties may play some role in the development and maintenance of seizures in this susceptible species. Parvalbumin immunoreactivity is rapidly and ephemerally increased in the hippocampus 15 min after reperfusion. Later on, there is a transitory decrease of parvalbumin immunoreactivity which is followed by an increase 6 h later in the stratum granulare hilus and CA3 area, and not until the first and second days in the CA1 area. This increase significantly surpasses the number of immunoreactive neurons in control animals in CA1 and CA3 from 48 h after reperfusion onwards. The effect is similar using different anaesthetics and does not occur in sham-operated animals. In contrast with these findings, the number of parvalbumin-immunoreactive neurons in the somatosensory cortex is not affected in our model of forebrain ischaemia. On the other hand, GABA-immunoreactive neurons in CA1 are preserved during the first week after reperfusion, although an increase in the number of these cells occurs at the end of this period. Delayed neuronal death occurs in the CA1 area 48 h after ischaemia, and marked reduction in the number of CA1 neurons is found by the end of the first week. Eighty per cent of the remaining cells in CA1 at day 7, and 83% at day 15, are parvalbumin-immunoreactive nonpyramidal neurons in contrast to 3% parvalbumin-immunoreactive cells in control animals. These findings indicate that GABAergic neurons in CA1 are preserved after forebrain ischaemia, and that parvalbumin in CA1 neurons is associated with survival.
在对照组以及通过双侧夹闭颈动脉造成20分钟前脑缺血的动物中,检测蒙古沙鼠(长爪沙鼠)海马体中的小白蛋白免疫反应性。与其他物种相比,沙鼠的海马体具有以下特征:(可能是兴奋性的)穿通通路的免疫反应性较强,而CA1区非锥体神经细胞(抑制性神经元)的免疫反应性较弱(神经元数量少且树突分支稀少)。这些特性可能在这个易感物种癫痫的发生和维持中发挥一定作用。再灌注15分钟后,海马体中的小白蛋白免疫反应性迅速短暂增加。随后,小白蛋白免疫反应性出现短暂下降,6小时后在颗粒层海马门和CA3区增加,直到第一天和第二天CA1区才增加。从再灌注48小时起,CA1和CA3区这种增加显著超过对照动物中免疫反应性神经元的数量。使用不同麻醉剂时效果相似,且在假手术动物中不出现。与这些发现相反,在我们的前脑缺血模型中,体感皮层中小白蛋白免疫反应性神经元的数量未受影响。另一方面,CA1区中GABA免疫反应性神经元在再灌注后的第一周内得以保留,尽管在此期间结束时这些细胞的数量有所增加。缺血48小时后CA1区发生迟发性神经元死亡,到第一周结束时发现CA1神经元数量明显减少。在第7天,CA1区剩余细胞的80%以及第15天的83%是小白蛋白免疫反应性非锥体神经元,而对照动物中只有3%的小白蛋白免疫反应性细胞。这些发现表明,前脑缺血后CA1区的GABA能神经元得以保留,并且CA1神经元中的小白蛋白与存活有关。