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Aim:To investigate the effect of l-stepholidine (SPD) on the frequency of spon-taneous excitatory postsynaptic currents (sEPSC) in the pyramidal cells betweenlayers Ⅴ and Ⅵ in the prelimbic cortex (PL).Methods:A whole-cell patch clamp inrat brain slices was used.Results:SPD significantly increased the frequency ofsEPSC in a concentration-dependent manner.A selective D_1 dopamine receptorantagonist SCH23390 blocked SPD-mediated effects,whereas the D_1 agonistSKF38393,but not the D_(2/3) antagonist sulpiride,mimicked SPD-mediated increasein the frequency of sEPSC.Moreover,both protein kinase A (PKA) inhibitor N-(2-[p-bromocinnamylamino]-ethyl)-5-isoquinolinesulfonamide hydrochloride andprotein kinase C (PKC) inhibitor chelerythrine attenuated the effect of SPD onsEPSC.Conelusion:SPD elicits its effect on the frequency of sEPSC on the PLpyramidal cells via presynaptic D_1 receptors,and is dependent on PKA and PKCsignaling pathways.
Aim: To investigate the effect of l-stepholidine (SPD) on the frequency of spon-taneous excitatory postsynaptic currents (sEPSC) in the pyramidal cells betweenlayers V and VI in the prelimbic cortex (PL). Methods: A whole- inrat 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, and the D_1 agonist SKF38393, but not the D_ (2/3) antagonist sulpiride, mimicked SPD-mediated increasein 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 onsEPSC.Conelusion: SPD elicits its effect on the frequency of sEPSC on the PLpyramidal cells via presynaptic D-1 receptors, and is dependent on PKA and PKCsignaling pathways.