Lancaster B, Wheal H V
Brain Res. 1984 Mar 19;295(2):317-24. doi: 10.1016/0006-8993(84)90980-6.
The chronic effects of the lesioning agent, kainic acid, on paired pulse inhibition in the CA1 area were investigated in the hippocampus both in vivo and in vitro. Pretreatment of animals with a unilateral intracerebroventricular (i.c.v.) injection of kainic acid resulted in a lesion of the CA3/4 area of the hippocampus ipsilateral to the injection site. On activating the surviving Schaffer collateral afferents in the contralateral hippocampus, normal paired-pulse inhibition of the extracellularly recorded population spike in CA1 was observed. On activating the surviving commissural afferents to the CA1 area ipsilateral to the lesion, no such inhibition could be observed. However, paired-pulse inhibition was recorded in the dentate gyrus ipsilateral to the lesion in response to stimulation of the perforant path. The chronic failure of inhibition following the unilateral i.c.v. injection of kainic acid further supports the use of this method to provide a chronic model in the rat for the study of epileptogenesis in the hippocampus.
研究了损伤剂 kainic 酸对海马体 CA1 区配对脉冲抑制的慢性影响，包括体内和体外实验。用单侧脑室内（i.c.v.）注射 kainic 酸对动物进行预处理，导致注射部位同侧海马体的 CA3/4 区损伤。在激活对侧海马体中存活的 Schaffer 侧支传入神经时，观察到 CA1 区细胞外记录的群体峰电位的正常配对脉冲抑制。在激活损伤同侧 CA1 区的存活连合传入神经时，未观察到这种抑制。然而，在损伤同侧的齿状回中，对穿通通路的刺激有配对脉冲抑制记录。单侧 i.c.v. 注射 kainic 酸后抑制的慢性失败进一步支持了使用该方法为大鼠提供慢性模型以研究海马体癫痫发生的研究。
