Epileptiform activities of pyramidal neurons in rat CA1 area induced by low-dosage veratridine
- VernacularTitle:小剂量藜芦碱诱发大鼠脑海马CA1区锥体神经元异常放电癫痫脑片模型的特征
- Author:
Gesheng LEI
;
Junling ZHU
;
Yehong WAN
;
Wenting WANG
;
Sanjue HU
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2005;9(25):238-239
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: The event of paroxysmal deplorizing shift (PDS) is the cellular hallmark of brain neurons of epileptiform activities. Its development used to be considered to be related to abnormal synaptic interactions. Recertly, the intrinsic nature of PDS has received more attention.OBJECTIVE: To observe the characteristics of epileptiform activities of rat hippocampal CA1 pyramidal neurons induced by low-dosage veratridine and investigate its possible ion mechanism.DESIGN: An exploratory and observational trial.SETTING: Institute of Neuroscience, Fourth Military Medical University of Chinese PLA.MATERIALS: This study was conducted at the Institute of Neuroscience,Fourth Military Medical University of Chinese PLA, from October 2002 to October 2004. Forty healthy SD rats of 14 days old were selected. Drugs were provided from Tianjin Drug Company and Sigma Company.METHODS: Rats were anesthetized by intraperitoneal injection, and their brain was removed and cut into slices. Epileptiform activities were induced by 0.5 μ mol/L veratridine. Then 80 nmol/L tetrodotoxin was added into the perfused solution on 6 cerebral slices, and 5 μmol/L phenytoin was used on another 5 cerebral slices. The electrophysiological characteristics of the cells under the effect of different kinds of drugs were observed.MAIN OUTCOME MEASURE: Discharge pattern of cells and tetrodotoxin-sensitive sodium currents under voltage-clamp configuration through Ⅰ-Ⅴ reaction.RESULTS: After perfusion of 0.5 μmol/L veratridine, the rat pyramidal neurons in CA1 area displayed relatively fixed-mode of runs of PDS bursting,followed by the hyperpolarization of cell membrane. Such epileptiform activities were blocked either by 80 nmol/L tetrodotoxin or 5 μnol/L phenytoin. The tetrodotoxin-sensitive sodium currents in epileptic neurons and normal controls under voltage-clamp configuration on holding potential of -55 rmV, -60 rmV, -65 mV. This shows that persistent sodium currents could be improved by low-dosage veratridine in a voltage-dependent manner.CONCLUSION: Low-dosage veratridine may induce runs of PDS like epileptiform activities on rat CA1 pyramidal neurons. Such changes can be blocked by low-dosage tetrodotoxin or phenytoin. Its ion mechanism may be related to persistent sodium currents.
