Cooperative activation of dopamine D1 and D2 receptors increases spike firing of nucleus accumbens neurons via G-protein betagamma subunits.

摘要: Dopamine in the nucleus accumbens modulates both motivational and addictive behaviors. D1 D2 receptors are generally considered to exert opposite effects at cellular level, but many behavioral studies find an apparent cooperative effect of accumbens. Here, we show that a dopamine-induced enhancement spike firing neurons brain slices required receptors. One intracellular mechanism might underlie cooperativity is activation specific subtypes adenylyl cyclases by G-protein betagamma subunits (Gbetagamma) released from Gi/o-linked receptor combination with Galpha(s)-like receptor. In this regard, dopaminergic was prevented inhibitors protein kinase A or Gbetagamma. Furthermore, perfusion Gbetagamma enabled not enhance firing. Finally, our data suggest these pathways may increase inhibition slow A-type potassium current. These results provide evidence for novel through which action could mediate dopamine-dependent