Jacobs K M, Gutnick M J, Prince D A
Department of Neurology and Neurological Sciences, Stanford University Medical Center, Stanford, CA 94305, USA.
Cereb Cortex. 1996 May-Jun;6(3):514-23. doi: 10.1093/cercor/6.3.514.
The presence of developmental cortical malformations has been associated with the occurrence of epilepsy, and correlative anatomic-clinical electrophysiological studies suggest that microdysgenic lesions may actually initiate epileptiform activity. We have investigated the electrophysiological properties of an animal model of polymicrogyria created by making cortical freeze lesions in rat pups at P0 or P1. Such lesions create microgyri with histological features similar to those of human polymicrogyria. We have determined that there is a focal region of hyperexcitability around the lesion in this rat microgyrus. Field potentials evoked by stimulation within a few millimeters of the microgyrus have characteristics typical of epileptiform activity. This aberrant activity is seen as early as 12 d after the lesion, as well as in animals as old as 118 d. Immunochemical staining for the calcium binding protein, parvalbumin, shows a decrease in neuronal and neuropil staining within the microgyrus. These findings suggest that inhibition might be decreased within the lesion, which may contribute to generation of the adjacent hyperexcitable region. These results demonstrate that this animal model is appropriate for examining the mechanisms contributing to epileptogenesis associated with a cortical malformation.
发育性皮质畸形的存在与癫痫的发生有关，相关的解剖学 - 临床电生理学研究表明，微小发育异常病变可能实际上引发癫痫样活动。我们研究了通过在出生后第0天或第1天对大鼠幼崽进行皮质冷冻损伤而创建的多小脑回动物模型的电生理特性。此类损伤产生的微小脑回具有与人多小脑回相似的组织学特征。我们已经确定，在这个大鼠微小脑回的损伤周围存在一个兴奋性过高的局灶区域。在微小脑回几毫米范围内进行刺激所诱发的场电位具有癫痫样活动的典型特征。这种异常活动早在损伤后12天就可见到，在118天大的动物中也可见到。对钙结合蛋白小白蛋白进行免疫化学染色显示，微小脑回内神经元和神经纤维网染色减少。这些发现表明，损伤内的抑制作用可能减弱，这可能有助于相邻兴奋性过高区域的产生。这些结果表明，这种动物模型适合用于研究与皮质畸形相关的癫痫发生机制。
