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Updated: Jun 29, 2026
Pentylenetetrazole-Induced Kindling Mouse Model
Published on: June 12, 2018
Enhanced synaptic vesicle traffic in hippocampus of phenytoin-resistant kindled rats
Kebin Zeng1, Xuefeng Wang, Yurong Wang
1Department of Neurology, The First Affiliated Hospital, Chongqing Medical University, Chongqing Key Laboratories of Neurology, Yuzhong, Chongqing, People's Republic of China. zkebin2008@yahoo.com.cn
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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