Dopamine D3 receptor modulates D2 receptor effects on cAMP and GABA release at striatopallidal terminals-Modulation by the Ca-Calmodulin-CaMKII system.

Dopamine D2 receptor (DR) is expressed in striatopallidal neurons and decreases forskolin-stimulated cyclic adenine monophosphate (cAMP) accumulation and gamma-aminobutyric acid (GABA) release. Dopamine D3 receptor (DR) mRNA is expressed in a population of striatal DR-expressing neurons. Also, DR protein and binding have been reported in the neuropil of globus pallidus.

Dopamine D4 receptor modulates inhibitory transmission in pallido-pallidal terminals and regulates motor behavior.

Two major groups of terminals release GABA within the Globus pallidus; one group is constituted by projections from striatal neurons, while endings of the intranuclear collaterals form the other one. Each neurons' population expresses different subtypes of dopamine D2-like receptors: D R subtype is expressed by encephalin-positive MSNs, while pallidal neurons express the D R subtype. The D R modulates the firing rate of striatal neurons and GABA release at their projection areas, while the D R regulates Globus pallidus neurons excitability and GABA release at their projection areas.

Cannabinoid-induced depression of synaptic transmission is switched to stimulation when dopaminergic tone is increased in the globus pallidus of the rodent.

Because activation of D2 receptors reverses the neurochemical effects of cannabinoids, we examined whether increasing dopaminergic tone in the globus pallidus (GPe) switches cannabinoid induced depression of synaptic transmission. GABAergic synaptic currents evoked in pallidal neurons by stimulation of striatal projections (IPSCs) were depressed by perfusion with the CB1R agonist ACEA. Coactivation of D2Rs with quinpirole converted the depression into stimulation.