左旋千金藤啶碱通过激活大鼠前边缘皮层神经元中的D1多巴胺信号通路增加微小兴奋性突触后电流的频率。
l-Stepholidine increases the frequency of sEPSC via the activation of D1 dopamine signaling pathway in rat prelimbic cortical neurons.
作者信息
Gao Ming, Liu Chang-Liang, Yang Shen, Zhen Xue-Chu, Jin Guo-Zhang
机构信息
Department of Pharmacology, State Key Laboratory of Drug Research, Institute of Materia Medica, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 201203, China.
出版信息
Acta Pharmacol Sin. 2007 May;28(5):627-33. doi: 10.1111/j.1745-7254.2007.00547.x.
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- [p-bromocinnamylamino]-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.
目的
研究左旋千金藤啶碱（SPD）对前边缘皮层（PL）V层和VI层之间锥体细胞自发兴奋性突触后电流（sEPSC）频率的影响。
方法
采用大鼠脑片全细胞膜片钳技术。
结果
SPD以浓度依赖性方式显著增加sEPSC频率。选择性D1多巴胺受体拮抗剂SCH23390可阻断SPD介导的效应，而D1激动剂SKF38393可模拟SPD介导的sEPSC频率增加，D2/3拮抗剂舒必利则不能。此外，蛋白激酶A（PKA）抑制剂N-（2-[对溴肉桂酰胺基]乙基）-5-异喹啉磺酰胺盐酸盐和蛋白激酶C（PKC）抑制剂白屈菜红碱均可减弱SPD对sEPSC的作用。
结论
SPD通过突触前D1受体对PL锥体细胞的sEPSC频率产生影响，且依赖于PKA和PKC信号通路。
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