GABAergic plasticity from PV interneurons onto pyramidal cells is associated with D1/D5 dopamine receptor signaling

<p><span style="font-family:&#39;calibri&#39; , sans-serif;font-size:11pt;letter-spacing:0px">Memory and learning processes are strongly modulated by dopamine;
consequently, its role in these processes has been extensively studied.
However, dopaminergic modulation of inhibitory transmission and synaptic
plasticity remains relatively underexplored compared with glutamatergic
transmission. In this study, the role of dopamine receptors (DRs) in the
regulation of inhibitory long-term plasticity at PV→PC synapses in the CA1
region was investigated. Blockade of DRs (SCH) converted iLTP to iLTD, whereas
receptor activation (SKF) abolished this form of plasticity. Furthermore, iLTP
was associated with prolonged eIPSC decay kinetics, an effect that was
abolished in the presence of either SCH or SKF. These findings suggest that
NMDA-dependent iLTP at PV→PC synapses is tightly regulated by dopaminergic
signalling.</span></p><p><br /></p>