Review: D1 dopamine receptor—the search for a function: A critical evaluation of the D1/D2 dopamine receptor classification and its functional implications

Abstract

The present review focuses on the hypothesized D1/D2 dopamine (DA) receptor classification, originally based on the form of receptor coupling to adenylate cyclase activity. The pharmacological effects of compounds exhibiting putative selective agonist or antagonist profiles at those DA receptors positively coupled to adenylate cyclase activity (D1 DA receptors) are extensively reviewed. Comparisons are made with the effects of putative selective D2 DA receptor agonists and antagonists, and on the basis of this work, the DA receptor classification is critically evaluated. A variety of biochemical, behavioral, and electrophysiological evidence is presented which supports the view that D1 and D2 DA receptors can interact in both an opposing and synergistic fashion. Particular attention is focused on the possibility that D1 receptor stimulation is required to enable the expression of certain D2 receptor-mediated effects, and the functional consequences of this form of interaction are considered. A hypothetical model is presented which considers how both the opposing and enabling forms of interaction between D1 and D2 DA receptors can control behavioral expression. Finally, the clinical relevance of this work is discussed and the potential use of selective D1 receptor agonists and antagonists in the treatment of psychotic states and Parkinson's disease is considered.

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D1 and D2 receptors

“…Although apparently puzzling, this D 1 /D 2 antagonist/antagonist interaction has been reported previously (for a review see Clark and White 1987). Indeed, SCH23390, ineffective alone, prevented the facilitation of striatal ACh (Saller and Salama 1986) and GABA (Harsing and Zigmond 1997) Effect of raclopride and SCH23390 on the NMDA-stimulated glutamate (GLU) release.…”

Sustained Withdrawal Allows Normalization of In Vivo [11C]N-Methylspiperone Dopamine D2 Receptor Binding after Chronic Binge Cocaine A Positron Emission Tomography Study in Rats

“…A study in rats using dopamine D 2 receptor antagonists showed that lower dopamine D 2 receptor availability does not alter cocaine self-administration (Caine and Koob 1994). However, the difference in recovery times for dopamine D 1 receptor binding versus dopamine D 2 receptor binding may lead to abnormalities in the putative opposing andրor synergistic relationships between dopamine D 1 and D 2 receptor subtypes (Clark and White 1987;Self et al 1996;Wang and McGinty 1997).…”

“…Microdialysis studies have shown that 22 hours following the last administration of chronic binge cocaine, baseline dopamine levels are significantly decreased, whereas cocaine continues to cause immediate elevations in striatal dopamine levels after each injection (Maisonneuve and Kreek 1994;Maisonneuve et al 1995). Increased activation of dopamine receptors by the increased concentrations of dopamine during cocaine administration may mediate many of cocaine's reinforcing effects (Ritz et al 1987;Clark and White 1987).…”

神经细胞中多巴胺d1和d5受体不同亚细胞分布和胞内转运的特性

“…With the advant of the D1 selective ligands, D1-like receptors are distinguished from the D2-like receptors [1][2][3] . Then D1-like receptor subtypes, D1 receptor (D1R) and D5 receptor (D5R), are further identified in mammalian brain by cDNA cloning [4][5][6][7] .…”