目的  了解小清蛋白(PV)、钙视网膜结合蛋白(CR)在皮质发育不良(CD)大鼠大脑皮质中的表达，探讨其在鉴别CD和参与癫痫发病机制中的作用。  方法  孕15d的SD大鼠腹腔注射卡莫司汀建立子代鼠CD模型，P30行热水浴诱发惊厥实验，组织病理学技术观察仔鼠皮质结构改变，免疫组化、免疫荧光、RT-PCR技术检测PV、CR在大鼠大脑皮质的表达。  结果   ①模型鼠热水浴诱发惊厥潜伏期缩短；②免疫组化示模型鼠大脑皮质PV阳性细胞数量[（77.50±4.49个）/视野] 较对照组[（37.28±2.72）个/视野] 减少（P<0.05）、空间分布紊乱、皮质浅层出现阳性细胞结节和阳性细胞空白区，CR的表达较对照组无显著差异；③免疫荧光示模型鼠PV阳性细胞减少,胞体增大；④RT-PCR检测示模型鼠PV mRNA相对表达量显著降低，CR mRNA的相对表达量无显著差异。  结论  PV可作为鉴定CD的指标；表达PV的GABA能抑制性中间神经元的损伤可能在CD所致的难治性癫痫中具有重要作用。

        Objective  To explore the expression of parvalbumin(PV) and calretinin(CR) in cerebral cortex of cortical dysplasia (CD) rats, and investigate their effects on pathogenesy of intractable epilepsy caused by CD.  Methods  Sprague-Dawley pregnant rats were given intraperitoneal injection of 1-3-bis-chloroethyl-　nitrosourea (BCNU) on embryonic day 15 (E15) for inducing CD in the offspring. The growth and development of rat brain and praxiology change of the offspring were analyzed adopting the warm-water-hyperspasmia inducing method. Cortical histopathology was examined in the resulting pups at postnatal 30 day (P30), at the same time, the expression of PV and CR in the cortex were explored by immunocytochemistry, Immunofluorescence and RT-PCR respectively.  Results   ① The latency period of hyperspasmia of CD animals was shorten; ② The density of PV positive cells in the cortex of model rats and controls were (37.28±2.72 )cells/ field and (77.50±4.49) cells/ field respectively, with the significance between them (P<0.05), followed by the altered spatial distribution, the appearance of PV positive cell aggregation or disappearence at the superficial layers of the cortex. However, there were no difference appeared between model and control animals for CR expression; ③The number of PV positive cells decreased, and the size of which increased in the Ⅳ layer of the cortex of CD rats; ④Relatively reduced expression of PV mRNA in cortex was detected in CD rat.  Conclusions  The PV can be used as a index to identify CD. Abnormal density and distribution of GABAergic interneurons which express PV in the CD model rats may play a pivotal role in the pathophysiologic mechanisms of intractable epilepsy .