Open Accessl ‐Stepholidine increases the frequency of sEPSC via the activation of D 1 dopamine signaling pathway in rat prelimbic cortical neurons 1
Author(s) -
GAO Ming,
LIU Changliang,
YANG Shen,
ZHEN Xuechu,
JIN Guozhang
Publication year - 2007
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2007.00547.x
Subject(s) - chelerythrine , protein kinase c , sulpiride , excitatory postsynaptic potential , agonist , chemistry , dopamine , antagonist , protein kinase a , infralimbic cortex , biophysics , pharmacology , endocrinology , medicine , receptor , kinase , biology , biochemistry , neuroscience , prefrontal cortex , cognition
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 D 1 dopamine receptor antagonist SCH23390 blocked SPD‐mediated effects, whereas the D 1 agonist SKF38393, but not the D 2/3 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 D 1 receptors, and is dependent on PKA and PKC signaling pathways.