[8] In mice, regulation of D2R surface expression by the neuronal calcium sensor-1 (NCS-1) in the dentate gyrus is involved in exploration, synaptic plasticity and memory formation.

[9] Studies have shown potential roles for D2R in retrieval of fear memories in the prelimbic cortex[10] and in discrimination learning in the nucleus accumbens.

[11] In flies, activation of the D2 autoreceptor protected dopamine neurons from cell death induced by MPP+, a toxin mimicking Parkinson's disease pathology.

The difference between the active and inactive of G protein-coupled receptor is mainly observed as conformational changes at the cytoplasmic half of the structure, particularly at the transmembrane domains (TM) 5 and 6.

[19] It was observed that either D2R agonist or antagonist ligands revealed better binding affinities inside the ligand-binding domain of the active D2R in comparison with the inactive state.

[citation needed] In order to assist in the management of these conditions, equilibration between the D2R states is controlled by implementing of agonist and antagonist D2R ligands.

[28] DRD2 TaqIA polymorphism has been reported to be associated with an increased risk for developing motor fluctuations but not hallucinations in Parkinson's disease.

[29][30] A splice variant in Dopamine receptor D2(rs1076560) was found to be associated with limb truncal tardive dyskinesia and diminished expression factor of Positive and Negative Syndrome Scale (PANSS) in schizophrenia subjects.