NMDA Receptors and Epileptogenesis in Human Cortical Dysplasia: A Metaanalysis
- *Corresponding Author:
- Jian Yin
Department of Neurosurgery
the Second Affiliated Hospital of Dalian Medical University
Liaoning, No. 467 Zhongshan Road, Shahekou District
Dalian 116023, People’s Republic of China
E-mail: [email protected]
Received Date: November 27, 2013; Accepted Date: December 23, 2013; Published Date: December 25, 2013
Citation: Yang K, Zhang C, Su J, Lang Y, Yin J (2013) NMDA Receptors and Epileptogenesis in Human Cortical Dysplasia: A Meta-analysis. J Cytol Histol 5:208. doi: 10.4172/2157-7099.1000208
Copyright: © 2013 2013 Yang K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Cortical dysplasia (CD) is a cerebral disorder caused by disruption of neuronal migration and disorganization of cortex development. The mechanisms of epileptogenicity in CD have been investigated yet still remain unknown. One of the possible reasons is the changes of expression of Nmethyl-D-aspartate (NMDA) receptors. Emerging evidences have shown that NR2A/B in the region of focal cortical dysplasia (FCD) cortex may play an important role in the risk of epilepsy and NR1 remains unchanged during epilepsy pathogenesis but recent published studies showed inconclusive results. This meta-analysis aimed to derive a more precise estimation of the associations between NMDA receptors and CD related epilepsy risk. A literature search of PubMed, Embase, Web of Science and China BioMedicine (CBM) databases was conducted on articles published before July 1st, 2013. Crude odds ratio (OR) with 95% confidence intervals (CI) were calculated. Ten studies were included with a total of 170 subjects. 104 of them were diagnosed with FCD and epilepsy while 66 resected specimen were non-CD cerebral tissue. The meta-analysis results showed that the expression of NR2B is increased in FCD cortex, which is indicated might be an important role in FCD related epilepsy pathogenesis. On the other hand, the expression of NR1 showed no significant difference between FCD group and controls, therefore the NR1 might not be a relevant factor. The function of NMDA receptors in development of FCD is not clear yet, a further explanation is still needed. We assume that NMDA receptors might interact with other substances in different signaling pathways to initiate and promote the epileptogenic process. Meanwhile we suggest more research to focus on the causal relationship between NMDA receptors and epileptogenisis.