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The adverse effects of pramipexole on probability discounting are not reversed by acute D<inf>2</inf> or D<inf>3</inf> receptor antagonism
2020, European NeuropsychopharmacologyCitation Excerpt :The mechanisms accounting for this up-regulation remain unclear, but they may partially reflect a compensatory response to significant changes in mesolimbic dopamine release. Indeed, we previously documented that the combination of RES and PPX reduced both phasic and tonic release of dopamine (Pes et al., 2017); accordingly, D3 receptor binding is markedly increased by dopamine depletion (Levant, 1995). However, these effects cannot fully account for the observed up-regulation of D3 receptors, given that our previous data showed that RES decreased dopamine release irrespective of its association with PPX (Pes et al., 2017).
Dopaminergic denervation switches dopamine D3 receptor signaling and disrupts its Ca<sup>2+</sup> dependent modulation by CaMKII and calmodulin in striatonigral projections of the rat
2015, Neurobiology of DiseaseCitation Excerpt :It remains for future research to elucidate which parameters of receptor–receptor interaction determine how activation of the same pair of receptors, D1 and D3, produces either synergistic or antagonistic effects in the same signaling cascade. Previous biochemical studies have shown enhanced D3R activity after DA depletion in different brain areas, including the striatum (Sato et al., 1994; Levant, 1995; Gurevich et al., 1999; Ishibashi et al., 2002). Our observations show that in addition to this effect, denervation switches signalization pathways in a single structure: the “atypical” mode in which D3Rs potentiates D1R activation at a site upstream of adenylyl cyclase (Avalos-Fuentes et al., 2013) becomes the “typical” inhibitory D2-like response after denervation (Figs. 1 and 2).
Positron emission tomography imaging of dopamine D<inf>2</inf> receptors using a highly selective radiolabeled D<inf>2</inf> receptor partial agonist
2013, NeuroImageCitation Excerpt :The observation that dopamine depletion did not change the binding potential of [11C]SV-III-130 in the caudate and putamen also suggests that endogenous dopamine has a low in vivo occupancy at D2 receptors. This result agrees well with previous reports that endogenous dopamine protects the D3 receptor (but not the D2 receptors) from alkylation by 1-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) and the spiperone analog, N-(p-isothiocyanatophenethyl)spiperone (NIPS) (Levant, 1995; Zhang et al., 1999). Occupancy of D3 receptors by endogenous dopamine in vivo is high due to the higher binding affinity of dopamine for dopamine D3 versus D2 receptors (Levant, 1997).
Positron emission tomographic evaluation of the putative dopamine-D3 receptor ligand, [<sup>11</sup>C]RGH-1756 in the monkey brain
2004, Neurochemistry International