Immunohistochemical investigation of voltage-gated potassium channel-interacting protein 1 in normal rat brain and Pentylenettrazole-induced seizures  

作　　者：Tao SU Ai-Hua LUO Wen-Dong CONG Wei-Wen SUN Wei-Yi DENG Qi-Hua ZHAO Zhuo-Hua ZHANG Wei-Ping LIAO 

机构地区：[1]Institute of Neuroscience and The Second Affiliated Hospital, Guangzhou Medical College, Guangzhou 510260, China [2]Center for Neuroscience and Aging, the Burnham Institute University of California, CA92037, San Diego, USA

出　　处：《Neuroscience Bulletin》2006年第4期195-203,共9页神经科学通报（英文版）

基　　金：National Nature Science Foundation of China （No. 30370503 and No. 30570642）.

摘　　要：Objective To explore the possible role of voltage-gated potassium channel-interacting protein 1 (KChIP1) in the pathogenesis of epilepsy. Methods Sprague Dawley female adult rats were treated with pentylenettrazole (PTZ) to develop acute and chronic epilepsy models. The approximate coronal sections of normal and epilepsy rat brain were processed for immunohistochemistry. Double-labeling confocal microscopy was used to determine the coexistence of KChIP1 and gamma-aminobutyric acid (GABA). Results KChIP1 was expressed abundantly throughout adult rat brain. KChIP1 is highly co-localize with GABA transmitter in hippocampus and cerebral cortex. In the acute PTZ-induced convulsive rats, the number of KChIP1-postive cells was significantly increased especially in the regions of CA1 and CA3 (P < 0.05); whereas the chronic PTZ-induced convulsive rats were found no changes. The number of GABA-labeled and co-labeled neurons in the hippocampus appeared to have no significant alteration responding to the epilepsy-genesis treatments. Conclusion KChIP1 might be involved in the PTZ-induced epileptogenesis process as a regulator to neuronal excitability through influencing the properties of potassium channels. KChIP1 is preferentially expressed in GABAergic neurons, but its changes did not couple with GABA in the epileptic models.Objective To explore the possible role of voltage-gated potassium channel-interacting protein 1 （KChIP1） in the pathogenesis of epilepsy. Methods Sprague Dawley female adult rats were treated with pentylenettrazole （PTZ） to develop acute and chronic epilepsy models. The approximate coronal sections of normal and epilepsy rat brain were processed for immunohistochemistry. Double-labeling confocal microscopy was used to determine the coexistence of KChIP1 and gamma-aminobutyric acid （GABA）. Results KChIP1 was expressed abundantly throughout adult rat brain. KChIP1 is highly co-localize with GABA transmitter in hippocampus and cerebral cortex. In the acute PTZ-induced convulsive rats, the number of KChIP 1-postive cells was significantly increased especially in the regions of CA 1 and CA3 （P 〈 0.05）; whereas the chronic PTZ-induced convulsive rats were found no changes. The number of GABA-labeled and co-labeled neurons in the hippocampus appeared to have no significant alteration responding to the epilepsy-genesis treatments. Conclusion KChIP1 might be involved in the PTZ-induced epileptogenesis process as a regulator to neuronal excitability through influencing the properties of potassium channels. KChIP1 is preferentially expressed in GABAergic neurons, but its changes did not couple with GABA in the epileptic models.

关 键 词：KChIP1 PTZ EPILEPSY SEIZURE GABA IMMUNOHISTOCHEMISTRY 

分 类 号：R741.02[医药卫生—神经病学与精神病学]