l-Stepholidine increases the frequency of sEPSC via the activation of D1 dopamine signaling pathway in rat prelimbic cortical neurons
Abstract
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 D1agonist 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.
Keywords:
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 D1agonist 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.