Abstract:

        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 .

Key words: Parvalbumin, Calretinin, Intractable epilepsy, 1-3-bis-chloroethyl-nitrosourea, Cortical dysplasia