I-Stepholidine increases the frequency of sEPSC via the activation of D_1 dopamine signaling pathway in rat prelimbic cortical neurons  

作　　者：Ming GAO Chang-liang LIU Shen YANG Xue-chu ZHEN Guo-zhang JIN 

机构地区：[1]Department of Pharmacology, State Key Laboratory of Drug Research, Institute of Materia Medica, Shanghai Institutes for BiologicalSciences, Chinese Academy of Sciences, Shanghai 201203, China

出　　处：《Acta Pharmacologica Sinica》2007年第5期627-633,共7页中国药理学报（英文版）

基　　金：the Ministry of Science and Technology(№ 973-2003CB5154000);the National Natural Science Foundation of China(№ 30271495,30230130)

摘　　要：Aim： To investigate the effect of l-stepholidine （SPD） on the frequency of spontaneous excitatory postsynaptic currents （sEPSC） in the pyramidal cells between layers Ⅴ and Ⅵ in the prelimbic cortex （PL）. Methods： A whole-cell patch clamp in rat brain slices was used. Results： SPD significantly increased the frequency of sEPSC in a concentration-dependent manner. A selective D1 dopamine receptor antagonist SCH23390 blocked SPD-mediated effects, whereas the D1 agonist SKF38393, but not the D2/3 antagonist sulpiride, mimicked SPD-mediated increase in the frequency of sEPSC. Moreover, both protein kinase A （PKA） inhibitor N-（2- Lo-bromocinnamylaminol-ethyl）-5-isoquinolinesulfonamide hydrochloride and protein kinase C （PKC） inhibitor chelerythrine attenuated the effect of SPD on sEPSC. Conclusion： SPD elicits its effect on the frequency of sEPSC on the PL pyramidal cells via presynaptic D1 receptors, and is dependent on PKA and PKC signaling pathways.Aim： To investigate the effect of l-stepholidine （SPD） on the frequency of spontaneous excitatory postsynaptic currents （sEPSC） in the pyramidal cells between layers Ⅴ and Ⅵ in the prelimbic cortex （PL）. Methods： A whole-cell patch clamp in rat brain slices was used. Results： SPD significantly increased the frequency of sEPSC in a concentration-dependent manner. A selective D1 dopamine receptor antagonist SCH23390 blocked SPD-mediated effects, whereas the D1 agonist SKF38393, but not the D2/3 antagonist sulpiride, mimicked SPD-mediated increase in the frequency of sEPSC. Moreover, both protein kinase A （PKA） inhibitor N-（2- Lo-bromocinnamylaminol-ethyl）-5-isoquinolinesulfonamide hydrochloride and protein kinase C （PKC） inhibitor chelerythrine attenuated the effect of SPD on sEPSC. Conclusion： SPD elicits its effect on the frequency of sEPSC on the PL pyramidal cells via presynaptic D1 receptors, and is dependent on PKA and PKC signaling pathways.

关 键 词：l-stepholidine prelimbic cortex whole-cellpatch clamp spontaneous excitatory postsynaptic currents dopamine receptor 

分 类 号：R285.5[医药卫生—中药学] R277.7[医药卫生—中医学]