کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3052655 | 1186117 | 2010 | 11 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Calretinin immunoreactivity in focal cortical dysplasias and in non-malformed epileptic cortex Calretinin immunoreactivity in focal cortical dysplasias and in non-malformed epileptic cortex](/preview/png/3052655.png)
SummaryFocal cortical dysplasias (FCDs) represent a prominent cause of pharmacologically intractable epilepsy. In FCD, the decrease of parvalbumin immunoreactive (PV+) inhibitory interneurons has been repeatedly documented. Here, we wanted to show whether another interneuronal population, the calretinin immunoreactive (CR+) neurons, exhibits any change in human FCD. We also investigated samples of morphologically normal temporal neocortex resected together with sclerotic hippocampus (nHSTN), where decrease of PV+ interneurons was previously documented as well. Brain tissue from 24 patients surgically treated for pharmacoresistant epilepsy was examined. Calretinin immunoreactivity was qualitatively evaluated and the density of CR+ neuronal profiles was quantified. As a control, post-mortem acquired neocortical samples of nine patients without any brain affecting disease were used.CR+ neurons were located predominantly in superficial cortical layers both in controls and pathological samples. Similarly, the morphology of CR+ neurons was unaffected in pathological samples. The overall density of CR+ neurons was significantly decreased in FCD type I (to approximately 70% of control values) and even more in FCD type II (to approximately 50% of controls). In nHSTN, no change compared to controls was found in CR+ neuronal density. Our results may contribute to the better understanding of the role of individual interneuronal populations in epileptogenesis.
Journal: Epilepsy Research - Volume 88, Issue 1, January 2010, Pages 76–86