Abstract
Aim: Intractable epilepsy is characterized of seizure resistance to the anti-epileptic drugs. The underlying mechanisms are still elusive. Alterations of synaptic vesicle traffic may be one of the candidate mechanisms. Methods: Phenytoin-resistant and phenytoin-non resistant epileptic rats were selected in the amygdala kindled adult male Wistar rats. Synaptotagmin-I and clathrin were determined by cDNA microarry analysis and Western blotting in the hippocampus of phenytoin-resistant and phenytoin-nonresistant kindled rats, which were associated with the exocytosis and endocytosis of the synaptic vesicle traffic. Results: Microarry analysis showed both synaptotagmin-I and clathrin mRNA were up-regulated at least 3.06 fold accompanied with their correspondent proteins increased by 52.3 ± 6.4 % and 76.7 ± 12.4 % respectively in the hippocampus of phenytoin-resistant rats as compared with those in phenytoin-nonresistant rats. There were no significant differences in plasma phenytoin concentrations between the two groups. Conclusions: The increased expressions of synaptotagmin-I and clathrin in the hippocampus of phenytoin-resistant kindled rats play a role in the development of intractable epilepsy.
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This work was supported by the Chinese National Institutes of Health Grants 98013457 to Dr. Xuefeng Wang and Natural Science Fund of Chongqing 08046 to Dr. Kebin Zeng.
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Zeng, K., Wang, X., Wang, Y. et al. Enhanced Synaptic Vesicle Traffic in Hippocampus of Phenytoin-Resistant Kindled Rats. Neurochem Res 34, 899–904 (2009). https://doi.org/10.1007/s11064-008-9856-9
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DOI: https://doi.org/10.1007/s11064-008-9856-9