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1
Jose, P. A., J. R. Raymond, M. D. Bates, A. Aperia, R. A. Felder, and R. M. Carey. "The renal dopamine receptors." Journal of the American Society of Nephrology 2, no. 8 (February 1992): 1265–78. http://dx.doi.org/10.1681/asn.v281265.
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Dopamine is an endogenous catecholamine that modulates many functions including behavior, movement, nerve conduction, hormone synthesis and release, blood pressure, and ion fluxes. Dopamine receptors in the brain have been classically divided into D1 and D2 subtypes, based on pharmacological data. However, molecular biology techniques have identified many more dopamine receptor subtypes. Several of the receptors cloned from the brain correspond to the classically described D1 and D2 receptors. Several D1 receptor subtypes have been cloned (D1A, D1B, and D5) and are each coupled to the stimulation of adenylyl cyclase. The D2 receptor has two isoforms, a shorter form, composed of 415 amino acids, is termed the D2short receptor. The long form, called the D2long receptor, is composed of 444 amino acids; both are coupled to the inhibition of adenylyl cyclase. The D3 and D4 receptors are closely related to, but clearly distinct from, the D2 receptor. They have not yet been linked to adenylyl cyclase activity. Outside of the central nervous system, the peripheral dopamine receptors have been classified into the DA1 and DA2 subtypes, on the basis of synaptic localization. The pharmacological properties of DA1 receptors roughly approximate those of D1 and D5 receptors, whereas those of DA2 receptors approximate those of D2 receptors. A renal dopamine receptor with some pharmacological features of the D2 receptor but not linked to adenylyl cyclase has been described in the renal cortex and inner medulla. In the inner medulla, this D2-like receptor, termed DA2k, is linked to stimulation of prostaglandin E2 production, apparently due to stimulation of phospholipase A2. Of the cloned dopamine receptors, only the mRNA of the D3 receptor has been reported in the kidney. The DA1 receptor in the kidney is associated with renal vasodilation and an increase in electrolyte excretion. The DA1-related vasodilation and inhibition of electrolyte transport is mediated by cAMP. The role of renal DA2 receptors remains to be clarified. Although DA1 and DA2 receptors may act in concert to decrease transport in the renal proximal convoluted tubule, the overall function of DA2 receptors may be actually the opposite of those noted for DA1 receptors. Dopamine has been postulated to act as an intrarenal natriuretic hormone. Moreover, an aberrant renal dopaminergic system may play a role in the pathogenesis of some forms of hypertension. A decreased renal production of dopamine and/or a defective transduction of the dopamine signal is/are present in some animal models of experimental hypertension as well as in some forms of human essential hypertension.
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Hussain, Tahir, and Mustafa F. Lokhandwala. "Renal Dopamine Receptors and Hypertension." Experimental Biology and Medicine 228, no. 2 (February 2003): 134–42. http://dx.doi.org/10.1177/153537020322800202.
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Dopamine has been recognized as an important modulator of central as well as peripheral physiologic functions in both humans and animals. Dopamine receptors have been identified in a number of organs and tissues, which Include several regions within the central nervous system, sympathetic ganglia and postganglionic nerve terminals, various vascular beds, the heart, the gastrointestinal tract, and the kidney. The peripheral dopamine receptors influence cardiovascular and renal function by decreasing afterload and vascular resistance and promoting sodium excretion. Within the kidney, dopamine receptors are present along the nephron, with highest density on proximal tubule epithelial cells. It has been reported that there is a defective dopamine receptor, especially D1 receptor function, in the proximal tubule of various animal models of hypertension as well as in humans with essential hypertension. Recent reports have revealed the site of and the molecular mechanisms responsible for the defect in D1 receptors in hypertension. Moreover, recent studies have also demonstrated that the disruption of various dopamine receptor subtypes and their function produces hypertension in rodents. In this review, we present evidence that dopamine and dopamine receptors play an important role in regulating renal sodium excretion and that defective renal dopamine production and/or dopamine receptor function may contribute to the development of various forms of hypertension.
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Awenowicz, Patrick W., and Linda L. Porter. "Local Application of Dopamine Inhibits Pyramidal Tract Neuron Activity in the Rodent Motor Cortex." Journal of Neurophysiology 88, no. 6 (December 1, 2002): 3439–51. http://dx.doi.org/10.1152/jn.00078.2002.
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Cortical neurons respond in a variety of ways to locally applied dopamine, perhaps because of the activation of different receptors within or among subpopulations of cells. This study was conducted to assess the effects of dopamine and the receptor subtypes that mediate the responses of a specific population of neurons, the pyramidal tract neurons (PTNs) in the rodent motor cortex. The specific subfamilies of dopamine receptors expressed by PTNs also were determined. PTNs were identified by antidromic stimulation in intact animals. Extracellular recordings of their spontaneous activity and glutamate-induced excitation were performed with multi-barrel pipettes to allow simultaneous recording and iontophoresis of several drugs. Prolonged (30 s) application of dopamine caused a progressive, nonlinear decrease in spontaneous firing rates for nearly all PTNs, with significant reductions from baseline spontaneous activity (71% of baseline levels) occurring between 20 and 30 s of iontophoresis. The D1 selective (SCH23390) and the D2 selective (eticlopride) antagonists were both effective in blocking dopamine-induced inhibition in nearly all PTNs. Mean firing levels were maintained within 3% of baseline levels during co-application of the D1 antagonist with dopamine and within 11% of baseline levels during co-application of the D2 antagonist and dopamine. SCH23390 was ineffective however, in 2 of 16 PTNs, and eticlopride was ineffective in 3 PTNs. The dopamine blockade by both antagonists in most neurons, along with the selective blockade by one, but not the other antagonist in a few neurons indicate that the overall population of PTNs exhibits a heterogeneous expression of dopamine receptors. The firing rate of PTNs was significantly enhanced by iontophoresis of glutamate (mean = 141% of baseline levels). These increases were attenuated significantly (mean= 98% of baseline) by co-application with dopamine in all PTNs, indicating dopaminergic interactions with glutamate transmission. The expression of dopamine receptors was studied with dual-labeling techniques. PTNs were identified by retrograde labeling with fast blue and the D1a, D2, or D5 receptor proteins were stained immunohistochemically. Some, but not all PTNs, showed labeling for D1a, D2, or D5 receptors. The D1a and D2 receptor immunoreactivity was observed primarily in the somata of PTNs, whereas D5 immunoreactivity extended well into the apical dendrites of PTNs. In accordance with findings of D1 and D2 receptor antagonism of dopamine's actions, the identification of three DA receptor subtypes on PTNs suggests that dopamine can directly modulate PTN activity through one or more receptor subtypes.
4
Zeng, Chunyu, and Pedro A. Jose. "Dopamine Receptors." Hypertension 57, no. 1 (January 2011): 11–17. http://dx.doi.org/10.1161/hypertensionaha.110.157727.
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Felder, R. A., C. C. Felder, G. M. Eisner, and P. A. Jose. "The dopamine receptor in adult and maturing kidney." American Journal of Physiology-Renal Physiology 257, no. 3 (September 1, 1989): F315—F327. http://dx.doi.org/10.1152/ajprenal.1989.257.3.f315.
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Dopamine, like other neurotransmitters, exerts its biological effects by occupation of specific receptor subtypes. The dopamine receptors in the central nervous system and certain endocrine organs are classified into the D1/D2 subtypes. Outside the central nervous system, the dopamine receptors are classified into the DA1/DA2 subtypes. The D1/D2 and DA1/DA2 receptor have marked similarities and some differences, the most notable of which is the lower affinity of the DA dopamine compared with the D dopamine receptor. DA1 receptor activation increases renal blood flow (RBF); stimulation of DA1 and DA2 receptors may also increase glomerular filtration rate (GFR). DA1 agonists inhibit fluid and electrolyte transport indirectly via hemodynamic mechanisms and directly by occupation of DA1 receptors in specific nephron segments. In the proximal tubule, DA1 agonists simulate adenylate cyclase and inhibit Na+-H+ antiport activity. They also increase phospholipase C and inhibit Na+-K+-ATPase activity (presumably as a consequence of protein kinase C activation). The latter effects may be facilitated by DA2 agonists. In cortical collecting ducts, dopamine antagonizes the effects of mineralocorticoids and the hydrosomotic effect of antidiuretic hormone. It has also been suggested that DA1 may also decrease sodium transport by influencing other hormones, such as atrial natriuretic peptide. Studies of dopamine in the young are complicated because of the propensity for dopamine to stimulate alpha-adrenoceptors. Dopamine alone may actually decrease RBF in the perinatal period. In some animals, the renal vasodilatory and natriuretic effects of dopamine increase with age. Renal tubular DA1-stimulated adenylate cyclase activity increases, whereas renal tubular DA1 receptors decrease with age. Renal DA2 receptor density is greater in the fetus; after birth renal DA2 receptors do not change. Endogenous dopamine may regulate sodium excretion in the young differently than in the adult. In the adult, sodium surfeit is associated with an increase in urinary dopamine; the opposite occurs in the young. A decrease in dopamine production or blockade of dopamine receptors results in an antinatriuresis in the adult; dopamine blockade in the young results in a natriuresis. It remains to be determined whether these age-related differences in dopamine effects are due to changes in receptor DA subtype density, second messengers, and/or interaction with other receptors.
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Chazot, P. L., A. J. Doherty, and P. G. Strange. "Antisera specific for D2 dopamine receptors." Biochemical Journal 289, no. 3 (February 1, 1993): 789–94. http://dx.doi.org/10.1042/bj2890789.
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Antisera have been raised against two peptides from the sequence of D2 dopamine receptors: peptide 1 from the predicted second extracellular loop and peptide 2 from the predicted third intracellular loop. The antisera recognize specifically a 95 kDa band in Western blots of several bovine brain regions, which corresponds to the denatured D2 dopamine receptor, whereas in recombinant CHO cells expressing D2 dopamine receptors a 80 kDa band is seen. The antisera immunoprecipitate 10-20% of the D2 dopamine receptors from soluble preparations of bovine brain. The antisera recognize D2 dopamine receptors in immunofluorescence analyses of recombinant CHO cells bearing the receptor gene. The antisera directed against the third intracellular loop, but not those against the second extracellular loop, will interfere with the coupling of D2 dopamine receptors and G-proteins in bovine brain preparations.
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Yamamoto, Kei, Romain Fontaine, Catherine Pasqualini, and Philippe Vernier. "Classification of Dopamine Receptor Genes in Vertebrates: Nine Subtypes in Osteichthyes." Brain, Behavior and Evolution 86, no. 3-4 (2015): 164–75. http://dx.doi.org/10.1159/000441550.
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Dopamine neurotransmission regulates various brain functions, and its regulatory roles are mediated by two families of G protein-coupled receptors: the D1 and D2 receptor families. In mammals, the D1 family comprises two receptor subtypes (D1 and D5), while the D2 family comprises three receptor subtypes (D2, D3 and D4). Phylogenetic analyses of dopamine receptor genes strongly suggest that the common ancestor of Osteichthyes (bony jawed vertebrates) possessed four subtypes in the D1 family and five subtypes in the D2 family. Mammals have secondarily lost almost half of the ancestral dopamine receptor genes, whereas nonmammalian species kept many of them. Although the mammalian situation is an exception among Osteichthyes, the current classification and characterization of dopamine receptors are based on mammalian features, which have led to confusion in the identification of dopamine receptor subtypes in nonmammalian species. Here we begin by reviewing the history of the discovery of dopamine receptors in vertebrates. The recent genome sequencing of coelacanth, gar and elephant shark led to the proposal of a refined scenario of evolution of dopamine receptor genes. We also discuss a current problem of nomenclature of dopamine receptors. Following the official nomenclature of mammalian dopamine receptors from D1 to D5, we propose to name newly identified receptor subtypes from D6 to D9 in order to facilitate the use of an identical name for orthologous genes among different species. To promote a nomenclature change which allows distinguishing the two dopamine receptor families, a nomenclature consortium is needed. This comparative perspective is crucial to correctly interpret data obtained in animal studies on dopamine-related brain disorders, and more fundamentally, to understand the characteristics of dopamine neurotransmission in vertebrates.
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Sunahara, Roger K., Philip Seeman, Hubert H. M. Van Tol, and Hyman B. Niznik. "Dopamine Receptors and Antipsychotic Drug Response." British Journal of Psychiatry 163, S22 (December 1993): 31–38. http://dx.doi.org/10.1192/s000712500029257x.
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Dopamine receptors have been divided into two major types – D1 and D2 – based primarily on pharmacological and biochemical criteria. Recent advances in the molecular biology of the dopamine receptor system have allowed the identification and characterisation of at least five distinct neuronal dopamine receptor genes (D1 to D5). These genes encode dopamine receptors belonging to the D1 receptor family, termed D1 and D5, and three D2-like receptors, termed D2, D3 and D4. These receptors are distinguished on the basis of their primary structure, chromosomal location, mRNA size and tissue distribution, and biochemical and pharmacological differences. Although individually these receptor subtypes may not be directly and exclusively involved in the maintenance or expression of schizophrenia, alterations of any of the receptors may contribute to the perturbation or instability of dopaminergic homeostasis in the brain. What was once thought to be a simple two-receptor system seems to have emerged as an intricate and interactive entity. This review summarises what is currently understood about dopamine receptors, their role in antipsychotic drug action, and their association with psychosis.
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Myslivecek, Jaromir. "Dopamine and Dopamine-Related Ligands Can Bind Not Only to Dopamine Receptors." Life 12, no. 5 (April 19, 2022): 606. http://dx.doi.org/10.3390/life12050606.
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The dopaminergic system is one of the most important neurotransmitter systems in the central nervous system (CNS). It acts mainly by activation of the D1-like receptor family at the target cell. Additionally, fine-tuning of the signal is achieved via pre-synaptic modulation by the D2-like receptor family. Some dopamine drugs (both agonists and antagonists) bind in addition to DRs also to α2-ARs and 5-HT receptors. Unfortunately, these compounds are often considered subtype(s) specific. Thus, it is important to consider the presence of these receptor subtypes in specific CNS areas as the function virtually elicited by one receptor type could be an effect of other—or the co-effect of multiple receptors. However, there are enough molecules with adequate specificity. In this review, we want to give an overview of the most common off-targets for established dopamine receptor ligands. To give an overall picture, we included a discussion on subtype selectivity. Molecules used as antipsychotic drugs are reviewed too. Therefore, we will summarize reported affinities and give an outline of molecules sufficiently specific for one or more subtypes (i.e., for subfamily), the presence of DR, α2-ARs, and 5-HT receptors in CNS areas, which could help avoid ambiguous results.
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Liggins, John. "Roles of Dopamine D1 and D2 Receptors in Working Memory Function." McGill Science Undergraduate Research Journal 4, no. 1 (March 31, 2009): 39–45. http://dx.doi.org/10.26443/msurj.v4i1.77.
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Dopamine has been implicated in the modulation of working memory via its interactions with circuits located in the prefrontal cortex of rodents and non-human primates. However, the role that pathways triggered by dopamine receptor subtypes play in affecting processes of working memory remains unclear. In humans, the evidence for dopaminergic modulation of working memory is controversial and the neurological substrates for dopamine’s modulatory effects are not fully understood. This paper will review the major animal and human studies that implicate synaptic dopaminergic transmission in working memory function and will outline a new framework to clarify the specific contribution of dopamine D2 receptors to the performance of this cognitive function. Specifically, it is proposed that activation of hippocampal dopamine D2 receptors by chemical agonists could result in the enhancement of spatial working memory.
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Zapata, Agustin, Bronwyn Kivell, Yang Han, Jonathan A. Javitch, Elizabeth A. Bolan, David Kuraguntla, Vanaja Jaligam, et al. "Regulation of Dopamine Transporter Function and Cell Surface Expression by D3 Dopamine Receptors." Journal of Biological Chemistry 282, no. 49 (October 8, 2007): 35842–54. http://dx.doi.org/10.1074/jbc.m611758200.
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D3 dopamine receptors are expressed by dopamine neurons and are implicated in the modulation of presynaptic dopamine neurotransmission. The mechanisms underlying this modulation remain ill defined. The dopamine transporter, which terminates dopamine transmission via reuptake of released neurotransmitter, is regulated by receptor- and second messenger-linked signaling pathways. Whether D3 receptors regulate dopamine transporter function is unknown. We addressed this issue using a fluorescent imaging technique that permits real time quantification of dopamine transporter function in living single cells. Accumulation of the fluorescent dopamine transporter substrate trans-4-[4-(dimethylamino)styryl]-1-methylpyridinium (ASP+) in human embryonic kidney cells expressing human dopamine transporter was saturable and temperature-dependent. In cells co-expressing dopamine transporter and D3 receptors, the D2/D3 agonist quinpirole produced a rapid, concentration-dependent, and pertussis toxin-sensitive increase of ASP+ uptake. Similar agonist effects were observed in Neuro2A cells and replicated in human embryonic kidney cells using a radioligand uptake assay in which binding to and activation of D3 receptors by [3H]dopamine was prevented. D3 receptor stimulation activated phosphoinositide 3-kinase and MAPK. Inhibition of either kinase prevented the quinpirole-induced increase in uptake. D3 receptor activation differentially affected dopamine transporter function and subcellular distribution depending on the duration of agonist exposure. Biotinylation experiments revealed that the rapid increase of uptake was associated with increased cell surface and decreased intracellular expression and increased dopamine transporter exocytosis. In contrast, prolonged agonist exposure reduced uptake and transporter cell surface expression. These results demonstrate that D3 receptors regulate dopamine transporter function and identify a novel mechanism by which D3 receptors regulate extracellular dopamine concentrations.
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Sobczuk, Paweł, Michał Łomiak, and Agnieszka Cudnoch-Jędrzejewska. "Dopamine D1 Receptor in Cancer." Cancers 12, no. 11 (November 2, 2020): 3232. http://dx.doi.org/10.3390/cancers12113232.
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Dopamine is a biologically active compound belonging to catecholamines. It plays its roles in the human body, acting both as a circulating hormone and neurotransmitter. It acts through G-protein-coupled receptors divided into two subgroups: D1-like receptors (D1R and D5R) and D2-like receptors (D2R, D3R, D4R). Physiologically, dopamine receptors are involved in central nervous system functions: motivation or cognition, and peripheral actions such as blood pressure and immune response modulation. Increasing evidence indicates that the dopamine D1 receptor may play a significant role in developing different human neoplasms. This receptor’s value was presented in the context of regulating various signaling pathways important in tumor development, including neoplastic cell proliferation, apoptosis, autophagy, migration, invasiveness, or the enrichment of cancer stem cells population. Recent studies proved that its activation by selective or non-selective agonists is associated with significant tumor growth suppression, metastases prevention, and tumor microvasculature maturation. It may also exert a synergistic anti-cancer effect when combined with tyrosine kinase inhibitors or temozolomide. This review provides a comprehensive insight into the heterogeneity of dopamine D1 receptor molecular roles and signaling pathways in human neoplasm development and discusses possible perspectives of its therapeutic targeting as an adjunct anti-cancer strategy of treatment. We highlight the priorities for further directions in this research area.
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Guidolin, Diego, Cinzia Tortorella, Manuela Marcoli, Chiara Cervetto, Raffaele De Caro, Guido Maura, and Luigi F. Agnati. "Modulation of Neuron and Astrocyte Dopamine Receptors via Receptor–Receptor Interactions." Pharmaceuticals 16, no. 10 (October 8, 2023): 1427. http://dx.doi.org/10.3390/ph16101427.
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Dopamine neurotransmission plays critical roles in regulating complex cognitive and behavioral processes including reward, motivation, reinforcement learning, and movement. Dopamine receptors are classified into five subtypes, widely distributed across the brain, including regions responsible for motor functions and specific areas related to cognitive and emotional functions. Dopamine also acts on astrocytes, which express dopamine receptors as well. The discovery of direct receptor–receptor interactions, leading to the formation of multimeric receptor complexes at the cell membrane and providing the cell decoding apparatus with flexible dynamics in terms of recognition and signal transduction, has expanded the knowledge of the G-protein-coupled receptor-mediated signaling processes. The purpose of this review article is to provide an overview of currently identified receptor complexes containing dopamine receptors and of their modulatory action on dopamine-mediated signaling between neurons and between neurons and astrocytes. Pharmacological possibilities offered by targeting receptor complexes in terms of addressing neuropsychiatric disorders associated with altered dopamine signaling will also be briefly discussed.
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Ashfaq, Muhammad, S. Mobasher Ali Abid, Khalid Rauf, Yasser Msa Alkahraman, Muhammad Zeeshan Haroon, Fawad Ahmad, Saima Ikram, and Jamshaid Ahmad. "Potential Role of Proton Pump Inhibitors Against Human DRD2 Receptor in Drug Induced Hyperprolactinemia." Revista de Chimie 71, no. 10 (November 3, 2020): 182–92. http://dx.doi.org/10.37358/rc.20.10.8362.
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Dopamine is a catecholamine neurotransmitter that control several important functions via different dopamine receptors(D1-D5). The Dopamine (DRD2) receptor and other D2 family receptors (D3 and D4) are predominantly involved in the inhibitory activities. One vital role of dopamine receptors is its involvement in the endocrine regulations including the hormone synthesis and their secretion. The regulation of prolactin hormone is mainly controlled through DRD2 receptors. Blocking the delivery of dopamine at these DRD2 receptors will cause an increase in serum prolactin levels. PPI�s are among the widely prescribed medications used for multiple gastric hypersecretory disorders and are shown to cause increase in serum prolactin level. This study focuses on computational methods to test PPIs interaction with dopamine D2 receptor through molecular docking & dynamics studies. The 3D structure of protein and the drugs were downloaded from PDB and PubChem databases. Protein and ligands were prepared followed by molecular docking. Complexes with best docking poses were then proceeded towards MD simulations of 60 ns. Results were then analyzed. This study confirmed that there is prospective affinity between proton pump inhibitors and dopamine D2 receptor, and dynamically stable complexes are formed after drug-receptor binding. MD simulations results confirmed the binding affinity between PPIs and Dopamine D2 receptor, concluding that the use of PPIs may be involved in drug induced hyperprolactinemia and other related effects.
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Bates, M. D., M. G. Caron, and J. R. Raymond. "Desensitization of DA1 dopamine receptors coupled to adenylyl cyclase in opossum kidney cells." American Journal of Physiology-Renal Physiology 260, no. 6 (June 1, 1991): F937—F945. http://dx.doi.org/10.1152/ajprenal.1991.260.6.f937.
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Peripheral dopamine receptors are classified as DA1 and DA2 receptors, similar to but distinct from central D1 and D2 receptors. Here we report the characterization of DA1 dopamine receptors in the opossum kidney (OK) cell line, which possesses properties of renal proximal tubule cells. OK cell membranes contain 248 +/- 12 fmol [125I]Sch 23982 binding sites/mg protein, which possess pharmacological properties appropriate for a DA1 receptor. Dopamine stimulates adenylyl cyclase via these receptors 4.3 +/- 0.4-fold (50% effective concentration = 4.0 +/- 0.7 microM). The responsiveness of this signaling system is regulated by agonist exposure. Exposure of these cells to dopamine leads to a rapid and profound desensitization of DA1-receptor-stimulated adenylyl cyclase that appears to be independent of the slower downregulation of DA1 receptors. Treatment of cells with 8-bromoadenosine 3',5'-cyclic monophosphate also desensitizes dopamine-stimulated adenylyl cyclase but in a fashion qualitatively and quantitatively distinct from that induced by agonist exposure. These data suggest that the cellular machinery for both homologous and heterologous desensitization of the DA1-receptor response exists in OK cells. Thus OK cells provide a model system for the study of the peripheral actions of dopamine at DA1 receptors and the regulation of these receptors.
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Mizuta, Kentaro, Yi Zhang, Dingbang Xu, Eiji Masaki, Reynold A. Panettieri, and Charles W. Emala. "The dopamine D2 receptor is expressed and sensitizes adenylyl cyclase activity in airway smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 302, no. 3 (February 1, 2012): L316—L324. http://dx.doi.org/10.1152/ajplung.00130.2011.
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Dopamine receptors are G protein-coupled receptors that are divided into two subgroups, “D1-like” receptors (D1 and D5) that couple to the Gs protein and “D2-like” receptors (D2, D3, and D4) that couple to Gi. Although inhaled dopamine has been reported to induce bronchodilation in patients with asthma, functional expression of dopamine receptor subtypes has never been described on airway smooth muscle (ASM) cells. Acute activation of Gi-coupled receptors inhibits adenylyl cyclase activity and cAMP synthesis, which classically impairs ASM relaxation. In contrast, chronic activation of Gi-coupled receptors produces a paradoxical enhancement of adenylyl cyclase activity referred to as heterologous sensitization. We questioned whether the dopamine D2-like receptor is expressed on ASM, whether it exhibits classical Gi-coupling, and whether it modulates ASM function. We detected the mRNA encoding the dopamine D2 receptor in total RNA isolated from native human ASM and from cultured human airway smooth muscle (HASM) cells. Immunoblots identified the dopamine D2 receptor protein in both native human and guinea pig ASM and cultured HASM cells. The dopamine D2 receptor protein was immunohistochemically localized to both human and guinea pig ASM. Acute activation of the dopamine D2 receptor by quinpirole inhibited forskolin-stimulated adenylyl cyclase activity in HASM cells, which was blocked by the dopamine D2 receptor antagonist L-741626. In contrast, the chronic pretreatment (1 h) with quinpirole potentiated forskolin-stimulated adenylyl cyclase activity, which was inhibited by L-741626, the phospholipase C inhibitor U73122, or the protein kinase C inhibitor GF109203X. Quinpirole also stimulated inositol phosphate synthesis, which was inhibited by L-741626 or U73122. Chronic pretreatment (1 h) of the guinea pig tracheal rings with quinpirole significantly potentiated forskolin-induced airway relaxation, which was inhibited by L-741626. These results demonstrate that functional dopamine D2 receptors are expressed on ASM and could be a novel therapeutic target for the relaxation of ASM.
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Bannon, Michael J., and Christopher J. Whitty. "Neurokinin receptor gene expression in substantia nigra: localization, regulation, and potential physiological significance." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 866–70. http://dx.doi.org/10.1139/y95-119.
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Neurokinin receptor gene expression within the rat and human substantia nigra was examined in detail. In the rat, the relative abundances of nigral neurokinin receptor mRNAs were neurokinin 3 > neurokinin 1 [Formula: see text] neurokinin 2. High levels of neurokinin 3 mRNA were localized to dopamine neurons, as determined by dopamine cell lesions and colocalization with tyrosine hydroxylase mRNA. Stimulation of nigral neurokinin 3 receptors activated dopamine cells, as evidenced by increases in striatal dopamine metabolism and in a postsynaptic measure of dopamine neurotransmission (i.e., striatal substance P encoding mRNA). These and other anatomical and physiological data suggest that in the rat, substance P (released from striatonigral neurons) may act on nigral nondopamine cells through neurokinin 1 receptors, while the substance P cotransmitter neurokinin A may act preferentially on nigral dopamine neurons through neurokinin 3 receptors. Interestingly, high levels of neurokinin 1 (but not neurokinin 3) receptor mRNA are seen within human substantia nigra dopamine cells. Thus drugs interacting with neurokinin receptors may prove to be of value in the treatment of various neuropsychiatric disorders.Key words: neurokinin receptor, mRNA, dopamine, substantia nigra, human.
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Ricci, Alberto, Sophie Marchal-Victorion, Elena Bronzetti, Angelo Parini, Francesco Amenta, and Seyed K. Tayebati. "Dopamine D4 Receptor Expression in Rat Kidney: Evidence for Pre- and Postjunctional Localization." Journal of Histochemistry & Cytochemistry 50, no. 8 (August 2002): 1091–96. http://dx.doi.org/10.1177/002215540205000811.
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Dopamine D4 receptors mediate inhibition of vasopressin-dependent sodium reabsorption by dopamine in collecting tubules. At present, the distribution of D4 receptors in other renal districts remains an open issue. The renal distribution of D4 receptor was assessed in normally innervated and denervated male Sprague-Dawley rats by quantitative immunohistochemistry using an anti-dopamine D4 receptor rabbit polyclonal antibody. D4 receptor protein immunoreactivity was observed perivascularly in the adventitia and the adventitia-media border. The density of perivascular dopamine D4 receptor was higher in afferent and efferent arterioles than in other segments of the renal vascular tree. Renal denervation abolished perivascular dopamine D4 receptor protein immunoreactivity. In renal tubules, the epithelium of collecting tubules showed the highest dopamine D4 receptor protein immunoreactivity, followed by the epithelium of proximal and distal tubules. No dopamine D4 receptor protein immunoreactivity was observed in the epithelium of the loop of Henle. Denervation did not change dopamine D4 receptor protein immunoreactivity in renal tubules. These results indicate that rat kidney expresses dopamine D4 receptors located both prejunctionally and nonprejunctionally in collecting, proximal, and distal tubules. This suggests that the dopamine D4 receptor may be involved in the control of neurotransmitter release and in renal hemodynamic and tubule function.
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Olesen, Kristin M., Heather M. Jessen, Catherine J. Auger, and Anthony P. Auger. "Dopaminergic Activation of Estrogen Receptors in Neonatal Brain Alters Progestin Receptor Expression and Juvenile Social Play Behavior." Endocrinology 146, no. 9 (September 1, 2005): 3705–12. http://dx.doi.org/10.1210/en.2005-0498.
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Abstract Steroid receptor activation in developing brain influences a variety of cellular processes that endure into adulthood, altering both behavior and physiology. We report that estrogen receptors can be activated in a ligand-independent manner within developing brain by membrane dopamine receptors. Neonatal treatment with either estradiol or a dopamine D1 receptor agonist can increase the expression of an estrogen receptor-regulated gene (i.e. progestin receptors) and later juvenile social play. More importantly, increases in social play behavior induced by neonatal treatment with estradiol or a dopamine D1 receptor agonist can be prevented by prior treatment with an estrogen receptor antagonist. This suggests that changes in dopamine transmission in developing brain can activate estrogen receptors in a ligand-independent manner to influence gene expression and have lasting consequences on social behavior.
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MISSALE, CRISTINA, S. RUSSEL NASH, SUSAN W. ROBINSON, MOHAMED JABER, and MARC G. CARON. "Dopamine Receptors: From Structure to Function." Physiological Reviews 78, no. 1 (January 1, 1998): 189–225. http://dx.doi.org/10.1152/physrev.1998.78.1.189.
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Missale, Cristina, S. Russel Nash, Susan W. Robinson, Mohamed Jaber, and Marc G. Caron. Dopamine Receptors: From Structure to Function. Physiol. Rev. 78: 189–225, 1998. — The diverse physiological actions of dopamine are mediated by at least five distinct G protein-coupled receptor subtypes. Two D1-like receptor subtypes (D1 and D5) couple to the G protein Gs and activate adenylyl cyclase. The other receptor subtypes belong to the D2-like subfamily (D2 , D3 , and D4) and are prototypic of G protein-coupled receptors that inhibit adenylyl cyclase and activate K+ channels. The genes for the D1 and D5 receptors are intronless, but pseudogenes of the D5 exist. The D2 and D3 receptors vary in certain tissues and species as a result of alternative splicing, and the human D4 receptor gene exhibits extensive polymorphic variation. In the central nervous system, dopamine receptors are widely expressed because they are involved in the control of locomotion, cognition, emotion, and affect as well as neuroendocrine secretion. In the periphery, dopamine receptors are present more prominently in kidney, vasculature, and pituitary, where they affect mainly sodium homeostasis, vascular tone, and hormone secretion. Numerous genetic linkage analysis studies have failed so far to reveal unequivocal evidence for the involvement of one of these receptors in the etiology of various central nervous system disorders. However, targeted deletion of several of these dopamine receptor genes in mice should provide valuable information about their physiological functions.
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Qaddumi, Waleed N., and Pedro A. Jose. "The Role of the Renal Dopaminergic System and Oxidative Stress in the Pathogenesis of Hypertension." Biomedicines 9, no. 2 (February 1, 2021): 139. http://dx.doi.org/10.3390/biomedicines9020139.
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The kidney is critical in the long-term regulation of blood pressure. Oxidative stress is one of the many factors that is accountable for the development of hypertension. The five dopamine receptor subtypes (D1R–D5R) have important roles in the regulation of blood pressure through several mechanisms, such as inhibition of oxidative stress. Dopamine receptors, including those expressed in the kidney, reduce oxidative stress by inhibiting the expression or action of receptors that increase oxidative stress. In addition, dopamine receptors stimulate the expression or action of receptors that decrease oxidative stress. This article examines the importance and relationship between the renal dopaminergic system and oxidative stress in the regulation of renal sodium handling and blood pressure. It discusses the current information on renal dopamine receptor-mediated antioxidative network, which includes the production of reactive oxygen species and abnormalities of renal dopamine receptors. Recognizing the mechanisms by which renal dopamine receptors regulate oxidative stress and their degree of influence on the pathogenesis of hypertension would further advance the understanding of the pathophysiology of hypertension.
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Ahangari, G., G. H. Shariati, M. R. Asadi, M. R. Ostadali, and H. R. Ahmadkhaniha. "Novel Mutation Detection of Regulatory Molecule Dopamine Gene Receptors (D1–D5) Encoding Analysis on Human Peripheral Blood Lymphocytes in Schizophrenia Patients." European Journal of Inflammation 7, no. 3 (September 2009): 145–52. http://dx.doi.org/10.1177/1721727x0900700304.
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There is much evidence which highlights the involvement of the dopamine system in the pathophysiology of schizophrenia. Recently, there have been reports of detected mutations in dopamine gene receptors in genomic DNA of schizophrenia. In this study, we attempt to determine whether there is mutation in encoding dopamine receptor. The PBMC was separated from whole blood by Ficoll-hypaque; the total cellular RNA was extracted and the cDNA was synthesized. This process followed by real-time PCR using primer pairs specific for five dopamine receptor mRNAs and β-actin as internal control. The results show the presence of all types of dopamine receptor types in lymphocytes. The mutational analysis of the obtained PCR products for the respective dopamine receptor fragments were analyzed by sequenced capillary system. The results presented in this study confirm the high frequency of mutations in dopamine gene receptor DRD5 in schizophrenia patients. Mutational amino acid changes in dopamine gene receptors of DR2, DR3, DR4 but not DR1 are also shown. In conclusion, this is the first report of such complete mutational analyses in all dopamine gene receptors. Moreover, we found new mutations and 80% frequency of mutations in DRD5. These data further strengthen the argument for the role of dopamine gene receptor mutations in the pathogenesis of schizophrenia.
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Trivedi, Meghna, Vihang A. Narkar, Tahir Hussain, and Mustafa F. Lokhandwala. "Dopamine recruits D1A receptors to Na-K-ATPase-rich caveolar plasma membranes in rat renal proximal tubules." American Journal of Physiology-Renal Physiology 287, no. 5 (November 2004): F921—F931. http://dx.doi.org/10.1152/ajprenal.00023.2004.
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Activation of dopamine D1A receptors in renal proximal tubules causes inhibition of sodium transporters (Na-K-ATPase and Na/H exchanger), leading to a decrease in sodium reabsorption. In addition to being localized on the plasma membrane, D1A receptors are mainly present in intracellular compartments under basal conditions. We observed, using [3H]SCH-23390 binding and immunoblotting, that dopamine recruits D1A receptors to the plasma membrane in rat renal proximal tubules. Furthermore, radioligand binding and/or immunoblotting experiments using pharmacological modulators showed that dopamine-induced D1A receptor recruitment requires activation of cell surface D1-like receptors, activation of adenylyl cyclase, and intact endocytic vesicles with internal acidic pH. A key finding of this study was that these recruited D1A receptors were functional because they potentiated dopamine-induced [35S]GTPγS binding, cAMP accumulation, and Na-K-ATPase inhibition. Interestingly, dopamine increased immunoreactivity of D1A receptors specifically in caveolin-rich plasma membranes isolated by a sucrose density gradient. In support of this observation, coimmunoprecipitation studies showed that D1A receptors interacted with caveolin-2 in an agonist-dependent fashion. The caveolin-rich plasma membranes had a high content of the α1-subunit of Na-K-ATPase, which is a downstream target of D1A receptor signaling in proximal tubules. These results show that dopamine, via the D1-like receptor-adenylyl cyclase pathway, recruits D1A receptors to the plasma membrane. These newly recruited receptors couple to G proteins, increase cAMP, and participate in dopamine-mediated inhibition of Na-K-ATPase in proximal tubules. Moreover, dopamine-induced recruitment of D1A receptors to the caveolin-rich plasma membranes brings them in close proximity to targets such as Na-K-ATPase in proximal tubules of Sprague-Dawley rats.
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Helms, My N., Xi-Juan Chen, Semra Ramosevac, Douglas C. Eaton, and Lucky Jain. "Dopamine regulation of amiloride-sensitive sodium channels in lung cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 4 (April 2006): L710—L722. http://dx.doi.org/10.1152/ajplung.00486.2004.
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Dopamine increases lung fluid clearance. This is partly due to activation of basolateral Na-K-ATPase. However, activation of Na-K-ATPase by itself is unlikely to produce large changes in transepithelial transport. Therefore, we examined apical and basolateral dopamine's effect on apical, highly selective sodium channels [epithelial sodium channels (ENaC)] in monolayers of an alveolar type 2 cell line (L2). Dopamine increased channel open probability ( Po) without changing the unitary current. The D1 receptor blocker SCH-23390 blocked the dopamine effect, but the D2 receptor blocker sulpiride did not. The dopamine-mediated increase in ENaC activity was not a secondary effect of dopamine stimulation of Na-K-ATPase, since ouabain applied to the basolateral surface to block the activity of Na-K-ATPase did not alter dopamine-mediated ENaC activity. Protein kinase A (PKA) was not responsible for dopamine's effect since a PKA inhibitor, H89, did not reduce dopamine's effect. However, cpt-2-O-Me-cAMP, which selectively binds and activates EPAC (exchange protein activated by cAMP) but not PKA, increased ENaC Po. An Src inhibitor, PP2, and the phosphatidylinositol-3-kinase inhibitor, LY-294002, blocked dopamine's effect on ENaC. In addition, an MEK blocker, U0126, an inhibitor of phospholipase A2, and a protein phosphatase inhibitor also blocked the effect of dopamine on ENaC Po. Finally, since the cAMP-EPAC-Rap1 pathway also activates DARPP32 (32-kDa dopamine response protein phosphatase), we confirmed that dopamine phosphorylates DARPP32, and okadaic acid, which blocks phosphatases (DARPP32), also blocks dopamine's effect. In summary, dopamine increases ENaC activity by a cAMP-mediated alternative signaling pathway involving EPAC and Rap1, signaling molecules usually associated with growth-factor-activated receptors.
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Zeng, Chunyu, Meng Zhang, Laureano D. Asico, Gilbert M. Eisner, and Pedro A. Jose. "The dopaminergic system in hypertension." Clinical Science 112, no. 12 (May 14, 2007): 583–97. http://dx.doi.org/10.1042/cs20070018.
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Dopamine plays an important role in the pathogenesis of hypertension by regulating epithelial sodium transport, vascular smooth muscle contractility and production of reactive oxygen species and by interacting with the renin–angiotensin and sympathetic nervous systems. Dopamine receptors are classified into D1-like (D1 and D5) and D2-like (D2, D3 and D4) subtypes based on their structure and pharmacology. Each of the dopamine receptor subtypes participates in the regulation of blood pressure by mechanisms specific for the subtype. Some receptors regulate blood pressure by influencing the central and/or peripheral nervous system; others influence epithelial transport and regulate the secretion and receptors of several humoral agents. This review summarizes the physiology of the different dopamine receptors in the regulation of blood pressure, and the relationship between dopamine receptor subtypes and hypertension.
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DeFrance, J. F., R. W. Sikes, and R. B. Chronister. "Dopamine action in the nucleus accumbens." Journal of Neurophysiology 54, no. 6 (December 1, 1985): 1568–77. http://dx.doi.org/10.1152/jn.1985.54.6.1568.
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The action of dopamine was studied in the nucleus accumbens of acutely prepared rabbits. Dopamine was applied iontophoretically to those cells and cell populations that responded in a monosynaptic excitatory manner to ipsilateral fimbrial stimulation. This strategy was adopted to isolate the effects of dopamine on postsynaptic receptors thus avoiding the bias resulting from activation of presynaptic dopamine receptors on dopaminergic afferents. Dopamine was found to have a suppressive effect on the excitatory (N) component of the field response and on driven extracellular unitary discharges. The specificity of dopamine's effect with receptors was indicated by the facts that fluphenazine effectively antagonized dopamine's effect, whereas bicuculline did not. The effect of dopamine was dependent on the rate of fimbrial stimulation. Dopamine has a marked suppressive effect on the fimbria-induced response at 0.5 Hz of stimulation but not at 6.0 Hz. This frequency specificity could not be linked directly to a cyclic adenosine 3',5'-cyclic monophosphate (cyclic AMP) mechanism because the iontophoresis cyclic AMP and dibutyryl cyclic AMP had suppressive effects at both 0.5 and 6.0 Hz rates of stimulation. It is suggested that dopamine acts in the nucleus accumbens to increase the "signal-to-noise" ratio. This might be a form of "contrast enhancement" of an incoming hippocampal message.
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Lokhandwala, Mustafa F., and Sharath S. Hegde. "Cardiovascular Dopamine Receptors: Role of Renal Dopamine and Dopamine Receptors in Sodium Excretion." Pharmacology & Toxicology 66, no. 4 (April 1990): 237–43. http://dx.doi.org/10.1111/j.1600-0773.1990.tb00741.x.
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Watanabe, Masayuki, Satoshi Tsuruta, Yasuhiro Inoue, Masayuki Kinuya, Kazuko Ogawa, Gunji Mamiya, and Toshihiko Tatsunuma. "Dopamine D1 and D2 receptors in spontaneously hypertensive rat brain striatum." Canadian Journal of Physiology and Pharmacology 67, no. 12 (December 1, 1989): 1596–97. http://dx.doi.org/10.1139/y89-256.
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Since it has been reported that dopamine D2 receptors are elevated in the brain striatum of spontaneously hypertensive (SH) rats, and since both D1 and D2 receptors may interact with one another, we measured the densities of both these receptors in SH rat striatum, as well as those in the normotensive Wistar–Kyoto rat striatum. The D1 receptor density in both strains was virtually the same, 72.9 ± 2.2 and 71.3 ± 3.2 pmol/g, respectively (mean ± SD). The D2 receptor densities were also almost identical, 16.3 ± 0.6 and 16.8 ± 1.0 pmol/g, respectively (mean ± SD). Thus, these data do not support the concept of a dopamine receptor related role in spontaneous hypertension.Key words: spontaneously hypertensive rat, D1 dopamine receptor, D2 dopamine receptor.
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Shaikh, Sanober, Andrew Makoff, David Collier, and Robert Kerwin. "Dopamine D4 Receptors." CNS Drugs 8, no. 1 (July 1997): 1–11. http://dx.doi.org/10.2165/00023210-199708010-00001.
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Levant, Beth, Zao Dung Ling, and Paul M. Carvey. "Dopamine D3 Receptors." CNS Drugs 12, no. 5 (1999): 391–402. http://dx.doi.org/10.2165/00023210-199912050-00006.
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Kohli, Jai D. "Peripheral Dopamine Receptors." American Journal of Hypertension 3, no. 6_Pt_2 (June 1990): 25S—28S. http://dx.doi.org/10.1093/ajh/3.6.25s.
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De Keyser, J., and G. Ebinger. "Neostriatal dopamine receptors." Trends in Neurosciences 13, no. 8 (August 1990): 324. http://dx.doi.org/10.1016/0166-2236(90)90138-z.
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Gerfen, Charles R., and Kristen A. Keefe. "Neostriatal dopamine receptors." Trends in Neurosciences 17, no. 1 (January 1994): 2–3. http://dx.doi.org/10.1016/0166-2236(94)90022-1.
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Bloch, Bertrand, and Catherine Le Moine. "Neostriatal dopamine receptors." Trends in Neurosciences 17, no. 1 (January 1994): 3–4. http://dx.doi.org/10.1016/0166-2236(94)90023-x.
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Helmeste, Daiga M., and Siu Wa Tang. "Dopamine D4 Receptors." Japanese Journal of Pharmacology 82, no. 1 (2000): 1–14. http://dx.doi.org/10.1254/jjp.82.1.
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Woodruff, G. N. "Dwindling dopamine receptors." Trends in Pharmacological Sciences 7 (January 1986): 252–53. http://dx.doi.org/10.1016/0165-6147(86)90338-x.
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Kebabian, John W. "Multiple Dopamine Receptors." Journal of Pharmaceutical Sciences 74, no. 8 (August 1985): 910–11. http://dx.doi.org/10.1002/jps.2600740842.
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Kandasamy, Krishnaveni, Abinaya Paramanandham, Goshika Russel Suthi Kumari, and Kameswaran Ramalingam. "A comprehensive review on the role of dopamine in the pathophysiology of tardive dyskinesia." International Journal of Research in Medical Sciences 11, no. 10 (September 29, 2023): 3925–30. http://dx.doi.org/10.18203/2320-6012.ijrms20233065.
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Tardive dyskinesia (TD) is a neurological syndrome characterized by involuntary, repetitive, and unusual movements that primarily impact the orofacial region while also extending to other body parts, encompassing chorea, dystonia, tics, buccolingual stereotypy, and akathisia. This condition stems from iatrogenic factors, particularly the chronic administration of medications that obstruct dopamine receptors. Predominantly implicated are antipsychotic drugs, utilized primarily for schizophrenia and bipolar disorder treatment. These drugs modulate dopamine levels, yet prolonged usage can induce alterations in dopamine receptor sensitivity and disruptions in dopaminergic pathways, consequently fostering TD. Dopamine, a pivotal neurotransmitter governing motor control, motivation, reward processing, and emotional regulation, exerts its effects through distinct dopamine receptor types, of which the D2 subtype assumes particular significance in TD development. The persistent blockade of D2 receptors by antipsychotics prompts a compensatory surge in receptor numbers and sensitivity, ultimately contributing to TD's emergence. In essence, TD reflects a complex interplay between medical intervention and neurological intricacies. The protracted influence of antipsychotics on dopamine receptors highlights the delicate equilibrium essential for optimal brain function. The unconventional movements characterizing TD underscore the intricate role of dopamine and its receptors in orchestrating neural equilibrium.
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Cheng, L., P. Precht, D. Frank, and C. T. Liang. "Dopamine stimulation of cAMP production in cultured opossum kidney cells." American Journal of Physiology-Renal Physiology 258, no. 4 (April 1, 1990): F877—F882. http://dx.doi.org/10.1152/ajprenal.1990.258.4.f877.
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Dopamine receptors have been identified in many tissues including the kidney. To establish an in vitro system as a model for dopamine action, we studied the effect of dopamine (DA) receptor agonists and antagonists on adenosine 3',5'-cyclic monophosphate (cAMP) formation in opossum kidney (OK) cells. The stimulation of cAMP production in these cells by dopamine was dose dependent, and markedly higher levels were observed in the presence of dopamine plus a phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine. Half-maximal stimulation was found with 1.15 +/- 0.22 microM dopamine. A DA1-receptor agonist, SKF 82526J, stimulated cAMP production, whereas a DA2-receptor agonist, Ly 171555, did not. The stimulatory effects of dopamine and SKF 82526J were abolished by a specific DA1-receptor antagonist, Sch 23390 with half-maximal inhibition concentrations of 1.24 +/- 0.18 and 4.0 +/- 0.5 nM, respectively. In contrast, the DA2-receptor antagonist, spiperone, had no inhibitory effect on dopamine- and SKF 82526J-stimulated cAMP production. Beta-Adrenergic antagonists failed to attenuate the stimulatory effects of dopamine and SKF 82526J on cAMP production. In addition, the beta-adrenergic receptor agonist, isoproterenol, did not stimulate cAMP production. These results suggest that the action of dopamine was not mediated through beta-adrenergic receptors. Furthermore, our results clearly demonstrated the existence of DA1-receptors linked to adenylate cyclase in OK cells.
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Ramanathan, Sankari, Tatiana Tkatch, Jeremy F. Atherton, Charles J. Wilson, and Mark D. Bevan. "D2-Like Dopamine Receptors Modulate SKCa Channel Function in Subthalamic Nucleus Neurons Through Inhibition of Cav2.2 Channels." Journal of Neurophysiology 99, no. 2 (February 2008): 442–59. http://dx.doi.org/10.1152/jn.00998.2007.
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The activity patterns of subthalamic nucleus (STN) neurons are intimately related to motor function/dysfunction and modulated directly by dopaminergic neurons that degenerate in Parkinson's disease (PD). To understand how dopamine and dopamine depletion influence the activity of the STN, the functions/signaling pathways/substrates of D2-like dopamine receptors were studied using patch-clamp recording. In rat brain slices, D2-like dopamine receptor activation depolarized STN neurons, increased the frequency/irregularity of their autonomous activity, and linearized/enhanced their firing in response to current injection. Activation of D2-like receptors in acutely isolated neurons reduced transient outward currents evoked by suprathreshold voltage steps. Modulation was inhibited by a D2-like receptor antagonist and occluded by voltage-dependent Ca2+ (Cav) channel or small-conductance Ca2+-dependent K+ (SKCa) channel blockers or Ca2+-free media. Because Cav channels are targets of Gi/o-linked receptors, actions on step- and action potential waveform-evoked Cav channel currents were studied. D2-like receptor activation reduced the conductance of Cav2.2 but not Cav1 channels. Modulation was mediated, in part, by direct binding of Gβγ subunits because it was attenuated by brief depolarization. D2 and/or D3 dopamine receptors may mediate modulation because a D4-selective agonist was ineffective and mRNA encoding D2 and D3 but not D4 dopamine receptors was detectable. Brain slice recordings confirmed that SKCa channel-mediated action potential afterhyperpolarization was attenuated by D2-like dopamine receptor activation. Together, these data suggest that D2-like dopamine receptors potently modulate the negative feedback control of firing that is mediated by the functional coupling of Cav2.2 and SKCa channels in STN neurons.
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Livingstone, C. D., P. G. Strange, and L. H. Naylor. "Molecular modelling of D2-like dopamine receptors." Biochemical Journal 287, no. 1 (October 1, 1992): 277–82. http://dx.doi.org/10.1042/bj2870277.
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Three-dimensional computer models of the rat D2, D3 and D4 dopamine receptor subtypes have been constructed based on the diffraction co-ordinates for bacteriorhodopsin, another membrane-bound protein containing seven transmembrane domains presumed to be arranged in a similar spatial orientation. Models were assembled by aligning the putative transmembrane domains of the dopamine receptors with those of bacteriorhodopsin using sequence similarities, and then superimposing these modelled alpha-helices on to the bacteriorhodopsin-derived co-ordinates. These models explore the potential hydrogen bonding, electrostatic and stacking interactions within the receptor which may be important for maintaining the conformation of these receptors, and thereby provide target sites for agonist binding. Proposed interactions between the catecholamine ligands and these receptors appear to account for the affinity, although not the specificity, of these agonist ligands for the different dopamine receptor subtypes. Such models will be useful for establishing structure-function relationships between ligands and the dopamine receptors, and may ultimately provide a template for the design of receptor-specific drugs.
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Vásquez, C., R. Navarro-Polanco, G. Hernández, J. Ruiz, D. G. Guerra, L. M. Baltazar, M. Huerta, and X. Trujillo. "Cannabinoids and Dopamine Receptors' Action on Calcium Current in Rat Neurons." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 32, no. 4 (May 2005): 529–37. http://dx.doi.org/10.1017/s031716710000456x.
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ABSTRACT:Objective:To study the effects of cannabinoid, glutamate, and dopamine agonists and antagonists on the calcium current in rat sympathetic neurons.Methods:Calcium current was recorded using the whole-cell variant of the patch-clamp technique. After expression in neuronal membranes of the cannabinoid CB1, glutamate mGluR2, or dopamine D1 receptor (by microinjection of the relevant receptor's cDNA into the neuron's nucleus) agonists' and antagonists' effects were observed.Results:Applications of agonists of the expressed receptor (0.1-10 µM) decreased the calcium current. The calcium current was increased after application of cannabinoid antagonists (AM251 and AM630); these compounds thus act as inverse agonists in this preparation. Glutamate and dopamine antagonists had no effects on the calcium current by themselves. Combined application of cannabinoids and dopamine, but not glutamate, agonists produced a decrement in the calcium current that was bigger than either of the effects seen when one agonist was applied alone.Conclusions:These results suggest that cannabinoid with dopamine receptors have an interactive inhibitory effect on the calcium current in this preparation, indicating that within the nervous system, receptor interactions may be important in the regulation of ion-channel functions.
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Tomassoni, Daniele, Enea Traini, Manuele Mancini, Vincenzo Bramanti, Syed Sarosh Mahdi, and Francesco Amenta. "Dopamine, vesicular transporters, and dopamine receptor expression in rat major salivary glands." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 309, no. 5 (September 2015): R585—R593. http://dx.doi.org/10.1152/ajpregu.00455.2014.
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The localization of dopamine stores and the expression and localization of dopamine (DAT) and vesicular monoamine transporters (VMAT) type-1 and -2 and of dopamine D1-like and D2-like receptor subtypes were investigated in rat submandibular, sublingual, and parotid salivary glands by HPLC with electrochemical detection, as well as immunochemical and immunohistochemical techniques. Male Wistar rats of 2 mo of age were used. The highest dopamine levels were measured in the parotid gland, followed by the submandibular and sublingual glands. Western blot analysis revealed DAT, VMAT-1, VMAT-2, and dopamine receptors immunoreactivity in membrane preparations obtained from the three glands investigated. Immunostaining for dopamine and transporters was developed within striated ducts. Salivary glands processed for dopamine receptors immunohistochemistry developed an immunoreaction primarily in striated and excretory ducts. In the submandibular gland, acinar cells displayed strong immunoreactivity for the D2 receptor, while cells of the convoluted granular tubules were negative for both D1-like and D2-like receptors. Parotid glands acinar cells displayed the highest immunoreactivity for both D1 and D2 receptors compared with other salivary glands. The above localization of dopamine and dopaminergic markers investigated did not correspond closely with neuron-specific enolase (NSE) localization. This indicates that at least in part, catecholamine stores and dopaminergic markers are independent from glandular innervation. These findings suggest that rat major salivary glands express a dopaminergic system probably involved in salivary secretion. The stronger immunoreactivity for dopamine transporters and receptors in striated duct cells suggests that the dopaminergic system could regulate not only quality, but also volume and ionic concentration of saliva.
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Kawahata, Ichiro, David I. Finkelstein, and Kohji Fukunaga. "Dopamine D1–D5 Receptors in Brain Nuclei: Implications for Health and Disease." Receptors 3, no. 2 (April 12, 2024): 155–81. http://dx.doi.org/10.3390/receptors3020009.
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Understanding the intricate role of dopamine D1–D5 receptors is pivotal in addressing the challenges posed by the aging global population, as well as by social stress and advancing therapeutic interventions. Central to diverse brain functions such as movement, cognition, motivation, and reward, dopamine receptors are ubiquitously distributed across various brain nuclei. This comprehensive review explores the nuanced functions of each dopamine receptor, D1, D2, D3, D4, and D5, in distinct brain regions, elucidating the alterations witnessed in several neurological and psychiatric disorders. From the substantia nigra and ventral tegmental area, crucial for motor control and reward processing, to the limbic system influencing emotional responses, motivation, and cognitive functions, each brain nucleus reveals a specific involvement of dopamine receptors. In addition, genetic variations in dopamine receptors affect the risk of developing schizophrenia and parkinsonism. The review further investigates the physiological significance and pathogenic impacts of dopamine receptors in critical areas like the prefrontal cortex, hypothalamus, and striatum. By unraveling the complexities of dopamine receptor biology, especially those focused on different brain nuclei, this review provides a foundation for understanding their varied roles in health and disease, which is essential for the development of targeted therapeutic strategies aimed at mitigating the impact of aging and mental health on neurological well-being.
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Zeng, Chunyu, Ines Armando, Yingjin Luo, Gilbert M. Eisner, Robin A. Felder, and Pedro A. Jose. "Dysregulation of dopamine-dependent mechanisms as a determinant of hypertension: studies in dopamine receptor knockout mice." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 2 (February 2008): H551—H569. http://dx.doi.org/10.1152/ajpheart.01036.2007.
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Dopamine plays an important role in the pathogenesis of hypertension by regulating epithelial sodium transport and by interacting with vasoactive hormones/humoral factors, such as aldosterone, angiotensin, catecholamines, endothelin, oxytocin, prolactin pro-opiomelancortin, reactive oxygen species, renin, and vasopressin. Dopamine receptors are classified into D1-like (D1 and D5) and D2-like (D2, D3, and D4) subtypes based on their structure and pharmacology. In recent years, mice deficient in one or more of the five dopamine receptor subtypes have been generated, leading to a better understanding of the physiological role of each of the dopamine receptor subtypes. This review summarizes the results from studies of various dopamine receptor mutant mice on the role of individual dopamine receptor subtypes and their interactions with other G protein-coupled receptors in the regulation of blood pressure.
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Wong, Franklin C., John Boja, Beng Ho, Michael J. Kuhar, and Dean F. Wong. "Affinity Labeling of Membrane Receptors Using Tissue-Penetrating Radiations." BioMed Research International 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/503095.
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Photoaffinity labeling, a usefulin vivobiochemical tool, is limited when appliedin vivobecause of the poor tissue penetration by ultraviolet (UV) photons. This study investigates affinity labeling using tissue-penetrating radiation to overcome the tissue attenuation and irreversibly label membrane receptor proteins. Using X-ray (115 kVp) at low doses (<50 cGy or Rad), specific and irreversible binding was found on striatal dopamine transporters with 3 photoaffinity ligands for dopamine transporters, to different extents. Upon X-ray exposure (115 kVp), RTI-38 and RTI-78 ligands showed irreversible and specific binding to the dopamine transporter similar to those seen with UV exposure under other conditions. Similarly, gamma rays at higher energy (662 keV) also affect irreversible binding of photoreactive ligands to peripheral benzodiazepine receptors (by PK14105) and to the dopamine (D2) membrane receptors (by azidoclebopride), respectively. This study reports that X-ray and gamma rays induced affinity labeling of membrane receptors in a manner similar to UV with photoreactive ligands of the dopamine transporter, D2 dopamine receptor (D2R), and peripheral benzodiazepine receptor (PBDZR). It may provide specific noninvasive irreversible block or stimulation of a receptor using tissue-penetrating radiation targeting selected anatomic sites.
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Barbanti, P., G. Fabbrini, A. Ricci, M. Paola Pascali, E. Bronzetti, F. Amenta, GL Lenzi, and R. Cerbo. "Migraine Patients Show an Increased Density of Dopamine D3 and D4 Receptors on Lymphocytes." Cephalalgia 20, no. 1 (February 2000): 15–19. http://dx.doi.org/10.1046/j.1468-2982.2000.00001.x.
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Recent studies have revealed peculiar functional and genetic features of dopamine receptors in migraine. As peripheral blood lymphocytes (PBL) may represent a tool for peripheral detection of neuroreceptors, we compared the expression of dopamine D3 (DRD3) and D4 (DRD4) receptors on PBL in migraine patients and in healthy controls using radioligand binding assay techniques in the presence of antidopamine D2-like receptor antibodies. The dopamine D2-like receptor agonist [3H]7-OH-DPAT was used as a radioligand. An increased density of both DRD3 ( P = 0.0006) and DRD4 ( P = 0.002) on PBL was observed in migraineurs compared with controls. This up-regulation might reflect central and/or peripheral dopamine receptor hypersensitivity due to hypofunction of the dopaminergic system. These findings support the view that dopamine D2-like receptors are involved in the determination of the so-called migraine trait, which may help to elucidate several clinical features of the disease.
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Garcia-Garrote, Maria, Juan A. Parga, Pablo J. Labandeira, Jose Luis Labandeira-Garcia, and Jannette Rodriguez-Pallares. "Dopamine Regulates Adult Neurogenesis in the Ventricular-Subventricular Zone via Dopamine D3 Angiotensin Type 2 Receptor Interactions." Stem Cells 39, no. 12 (September 20, 2021): 1778–94. http://dx.doi.org/10.1002/stem.3457.
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Abstract Adult neurogenesis is a dynamic and highly regulated process, and different studies suggest that dopamine modulates ventricular-subventricular zone (V-SVZ) neurogenesis. However, the specific role of dopamine and the mechanisms/factors underlying its effects on physiological and pathological conditions such as Parkinson's disease (PD) are not fully understood. Recent studies have described counter-regulatory interactions between renin-angiotensin system (RAS) and dopamine in peripheral tissues and in the nigrostriatal system. We have previously demonstrated that angiotensin receptors regulate proliferation and generation of neuroblasts in the rodent V-SVZ. However, possible interactions between dopamine receptors and RAS in the V-SVZ and their role in alterations of neurogenesis in animal models of PD have not been investigated. In V-SVZ cultures, activation of dopamine receptors induced changes in the expression of angiotensin receptors. Moreover, dopamine, via D2-like receptors and particularly D3 receptors, increased generation of neurospheres derived from the V-SVZ and this effect was mediated by angiotensin type-2 (AT2) receptors. In rats, we observed a marked reduction in proliferation and generation of neuroblasts in the V-SVZ of dopamine-depleted animals, and inhibition of AT1 receptors or activation of AT2 receptors restored proliferation and generation of neuroblasts to control levels. Moreover, intrastriatal mesencephalic grafts partially restored proliferation and generation of neuroblasts observed in the V-SVZ of dopamine-depleted rats. Our data revealed that dopamine and angiotensin receptor interactions play a major role in the regulation of V-SVZ and suggest potential beneficial effects of RAS modulators on the regulation of adult V-SVZ neurogenesis.
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Giorgioni, Gianfabio. "Receptors in Aging Diseases: Dopamine Receptors." Medicinal Chemistry Research 13, no. 1-2 (January 2004): 103–4. http://dx.doi.org/10.1007/s00044-004-0015-9.
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Ford, Christopher P., Michael J. Beckstead, and John T. Williams. "Kappa Opioid Inhibition of Somatodendritic Dopamine Inhibitory Postsynaptic Currents." Journal of Neurophysiology 97, no. 1 (January 2007): 883–91. http://dx.doi.org/10.1152/jn.00963.2006.
Full textAbstract:
In the midbrain, dopamine neurons can release dopamine somatodendritically. This results in an inhibitory postsynaptic current (IPSC) within adjacent dopamine cells that occurs by the activation of inhibitory D2 autoreceptors. Kappa, but not mu/delta, opioid receptors inhibit this IPSC. The aim of the present study was to determine the mechanism by which κ-opioid receptors inhibit the dopamine IPSC. In both the ventral tegmental area (VTA) and substantia nigra compacta (SNc) the κ-receptor agonist U69593 inhibited the IPSC, but not the current induced by the exogenous iontophoretic application of dopamine. The endogenous peptide dynorphin A (1–13) also inhibited IPSCs in the VTA and SNc, but also the dopamine iontophoretic current in the VTA. Although both kappa agonists induced a postsynaptic outward current in the VTA, the current induced by dynorphin was dramatically larger. This suggests that the decrease in iontophoretic dopamine current was the result of occlusion. Occlusion alone, however, could not completely account for suppression of the IPSC. The kappa opioid inhibition of the IPSC was not affected by global increases or decreases in dopamine cell activity within the slice. These findings suggest that, although kappa opioid receptors can hyperpolarize dopamine neurons, they also suppress dopamine release by direct actions at the release site. The results thus demonstrate both pre- and postsynaptic actions of kappa receptor agonists. The actions of dynorphin indicate that VTA dopamine cells are selectively regulated by kappa receptors.