Academic literature on the topic 'D1-class receptor'
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Journal articles on the topic "D1-class receptor"
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Watanabe, Katsushige, and Minoru Kimura. "Dopamine Receptor–Mediated Mechanisms Involved in the Expression of Learned Activity of Primate Striatal Neurons." Journal of Neurophysiology 79, no. 5 (May 1, 1998): 2568–80. http://dx.doi.org/10.1152/jn.1998.79.5.2568.
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Watanabe, Katsushige and Minoru Kimura. Dopamine receptor–mediated mechanisms involved in the expression of learned activity of primate striatal neurons. J. Neurophysiol. 79: 2568–2580, 1998. To understand the mechanisms by which basal ganglia neurons express acquired activities during and after behavioral learning, selective dopamine (DA) receptor antagonists were applied while recording the activity of striatal neurons in monkeys performing behavioral tasks. In experiment 1, a monkey was trained to associate a click sound with a drop of reward water. DA receptor antagonists were administered by micropressure using a stainless steel injection cannula (300 μm ID) through which a Teflon-coated tungsten wire for recording neuronal activity had been threaded. Responses to sound by tonically active neurons (TANs), a class of neurons in the primate striatum, were recorded through a tungsten wire electrode during the application of either D1- or D2-class DA receptor antagonists (total volume <1 μl, at a rate of 1 μl/5–10 min). Application of the D2-class antagonist, (−)-sulpiride (20 μg/μl, 58 mM, pH 6.8), abolished the responses of four of five TANs examined. In another five TANs, neither the D2-class antagonist nor the D1-class antagonists, SCH23390 (10 μg/μl, 31 mM, pH 5.7) or cis-flupenthixol (30 μg/μl, 59 mM, pH 6.6) significantly suppressed responses. In experiment 2, four- or five-barreled glass microelectrodes were inserted into the striatum. The central barrel was used for extracellular recording of activity of TANs. Each DA receptor antagonist was iontophoretically applied through one of the surrounding barrels. SCH23390 (10 mM, pH 4.5) and (−)-sulpiride (10 mM, pH 4.5) were used. The effects of iontophoresis of both D1- and D2-class antagonists were examined in 40 TANs. Of 40 TANs from which recordings were made, responses were suppressed exclusively by the D2-class antagonist in 19 TANs, exclusively by the D1-class antagonist in 3 TANs, and by both D1- and D2-class antagonists in 7 TANs. When 0.9% NaCl, saline, was applied by pressure (<1 μl) or by iontophoresis (<30 nA) as a control, neither the background discharge rates nor the responses of TANs were significantly influenced. Background discharge rate of TANs was also not affected by D1- or D2-class antagonists applied by either micropressure injection or iontophoresis. It was concluded that the nigrostriatal DA system enables TANs to express learned activity primarily through D2-class and partly through D1-class receptor–mediated mechanisms in the striatum.
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Ibañez-Sandoval, Osvaldo, Adán Hernández, Benjamin Florán, Elvira Galarraga, Dagoberto Tapia, Rene Valdiosera, David Erlij, Jorge Aceves, and José Bargas. "Control of the Subthalamic Innervation of Substantia Nigra Pars Reticulata by D1 and D2 Dopamine Receptors." Journal of Neurophysiology 95, no. 3 (March 2006): 1800–1811. http://dx.doi.org/10.1152/jn.01074.2005.
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The effects of activating dopaminergic D1 and D2 class receptors of the subthalamic projections that innervate the pars reticulata of the subtantia nigra (SNr) were explored in slices of the rat brain using the whole cell patch-clamp technique. Excitatory postsynaptic currents (EPSCs) that could be blocked by 6-cyano-7-nitroquinoxalene-2,3-dione and d-(−)-2-amino-5-phosphonopentanoic acid were evoked onto reticulata GABAergic projection neurons by local field stimulation inside the subthalamic nucleus in the presence of bicuculline. Bath application of ( RS)-2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine hydrochloride (SKF-38393), a dopaminergic D1-class receptor agonist, increased evoked EPSCs by ∼30% whereas the D2-class receptor agonist, trans-(−)-4aR-4,4a,5,6,7,8,8a,9-octahydro-5-propyl-1H-pyrazolo(3,4-g)quinoline (quinpirole), reduced EPSCs by ∼25%. These apparently opposing actions were blocked by the specific D1- and D2-class receptor antagonists: R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetra-hydro-1H-3-benzazepinehydrochloride (SCH 23390) and S-(−)-5-anino-sulfonyl- N-[(1-ethyl-2-pyrrolidinyl)-methyl]-2-methoxybenzamide (sulpiride), respectively. Both effects were accompanied by changes in the paired-pulse ratio, indicative of a presynaptic site of action. The presynaptic location of dopamine receptors at the subthalamonigral projections was confirmed by mean-variance analysis. The effects of both SKF-38393 and quinpirole could be observed on terminals contacting the same postsynaptic neuron. Sulpiride and SCH 23390 enhanced and reduced the evoked EPSC, respectively, suggesting a constitutive receptor activation probably arising from endogenous dopamine. These data suggest that dopamine presynaptically modulates the subthalamic projection that targets GABAergic neurons of the SNr. Implications of this modulation for basal ganglia function are discussed.
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Wang, Chenguang, Nagarajan Pattabiraman, Jian Nian Zhou, Maofu Fu, Toshiyuki Sakamaki, Chris Albanese, Zhiping Li, et al. "Cyclin D1 Repression of Peroxisome Proliferator-Activated Receptor γ Expression and Transactivation." Molecular and Cellular Biology 23, no. 17 (September 1, 2003): 6159–73. http://dx.doi.org/10.1128/mcb.23.17.6159-6173.2003.
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ABSTRACT The cyclin D1 gene is overexpressed in human breast cancers and is required for oncogene-induced tumorigenesis. Peroxisome proliferator-activated receptor γ (PPARγ) is a nuclear receptor selectively activated by ligands of the thiazolidinedione class. PPARγ induces hepatic steatosis, and liganded PPARγ promotes adipocyte differentiation. Herein, cyclin D1 inhibited ligand-induced PPARγ function, transactivation, expression, and promoter activity. PPARγ transactivation induced by the ligand BRL49653 was inhibited by cyclin D1 through a pRB- and cdk-independent mechanism, requiring a region predicted to form an helix-loop-helix (HLH) structure. The cyclin D1 HLH region was also required for repression of the PPARγ ligand-binding domain linked to a heterologous DNA binding domain. Adipocyte differentiation by PPARγ-specific ligands (BRL49653, troglitazone) was enhanced in cyclin D1−/− fibroblasts and reversed by retroviral expression of cyclin D1. Homozygous deletion of the cyclin D1 gene, enhanced expression by PPARγ ligands of PPARγ and PPARγ-responsive genes, and cyclin D1−/− mice exhibit hepatic steatosis. Finally, reduction of cyclin D1 abundance in vivo using ponasterone-inducible cyclin D1 antisense transgenic mice, increased expression of PPARγ in vivo. The inhibition of PPARγ function by cyclin D1 is a new mechanism of signal transduction cross talk between PPARγ ligands and mitogenic signals that induce cyclin D1.
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Yamamoto, Kei, Olivier Mirabeau, Charlotte Bureau, Maryline Blin, Sophie Michon-Coudouel, Michaël Demarque, and Philippe Vernier. "Evolution of Dopamine Receptor Genes of the D1 Class in Vertebrates." Molecular Biology and Evolution 30, no. 4 (November 28, 2012): 833–43. http://dx.doi.org/10.1093/molbev/mss268.
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Sasikumar, T. K., D. A. Burnett, H. Zhang, A. Smith-Torhan, A. Fawzi, and J. E. Lachowicz. "Hydrazides of clozapine: A new class of D1 dopamine receptor subtype selective antagonists." Bioorganic & Medicinal Chemistry Letters 16, no. 17 (September 2006): 4543–47. http://dx.doi.org/10.1016/j.bmcl.2006.06.022.
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Vargo, J. M., B. B. Bromberg, P. J. Best, J. V. Corwin, and J. F. Marshall. "D1-class dopamine receptor involvement in the behavioral recovery from prefrontal cortical injury." Behavioural Brain Research 72, no. 1-2 (December 1995): 39–48. http://dx.doi.org/10.1016/0166-4328(95)00028-3.
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Shayegan, Darius K., and Stephen M. Stahl. "Atypical Antipsychotics: Matching Receptor Profile to Individual Patient's Clinical Profile." CNS Spectrums 9, S11 (October 2004): 6–14. http://dx.doi.org/10.1017/s1092852900025086.
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AbstractUnderstanding common pharmacologic and clinical “class” actions associated with atypical antipsychotics certainly reveals how these agents are alike, but what about unique differences from one agent to another? Atypical antipsychotics are also a heterogeneous group of agents that have complex pharmacologic entities, acting upon multiple dopamine receptors (D2, D1 (D3, and D4) and multiple serotonin receptors (5-HT2A, 5-HT2C, 5-HT1A, and 5-HT1D, among others). Atypical antipsychotics also interact with noradrenergic (α1- and α2-adrenergic receptor blockade), histaminergic (H1-receptor blockade), and cholinergic (muscarinic M1 blockade) neurotransmitter systems as well as with monoamine (D, 5-HT, and norepinephrine reuptake blockade) transporters. However, no two atypical antipsychotics possess the same portfolio of actions upon all of these additional neurotransmitter systems.
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Sakurai, Atsuko, Julie Gavard, Yuliya Annas-Linhares, John R. Basile, Panomwat Amornphimoltham, Todd R. Palmby, Hiroshi Yagi, et al. "Semaphorin 3E Initiates Antiangiogenic Signaling through Plexin D1 by Regulating Arf6 and R-Ras." Molecular and Cellular Biology 30, no. 12 (April 12, 2010): 3086–98. http://dx.doi.org/10.1128/mcb.01652-09.
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ABSTRACT Recent studies revealed that a class III semaphorin, semaphorin 3E (Sema3E), acts through a single-pass transmembrane receptor, plexin D1, to provide a repulsive cue for plexin D1-expressing endothelial cells, thus providing a highly conserved and developmentally regulated signaling system guiding the growth of blood vessels. We show here that Sema3E acts as a potent inhibitor of adult and tumor-induced angiogenesis. Activation of plexin D1 by Sema3E causes the rapid disassembly of integrin-mediated adhesive structures, thereby inhibiting endothelial cell adhesion to the extracellular matrix (ECM) and causing the retraction of filopodia in endothelial tip cells. Sema3E acts on plexin D1 to initiate a two-pronged mechanism involving R-Ras inactivation and Arf6 stimulation, which affect the status of activation of integrins and their intracellular trafficking, respectively. Ultimately, our present study provides a molecular framework for antiangiogenesis signaling, thus impinging on a myriad of pathological conditions that are characterized by aberrant increase in neovessel formation, including cancer.
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Prommer, Eric. "Olanzapine." American Journal of Hospice and Palliative Medicine® 30, no. 1 (April 10, 2012): 75–82. http://dx.doi.org/10.1177/1049909112441241.
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Olanzapine is an atypical antipsychotic agent of the thienobenzodiazepine class. Olanzapine blocks multiple neurotransmitter receptors, including dopaminergic (D1, D2, D3, and D4), serotonergic (5-hydroxytryptamine 2A [5-HT2A], 5-HT2C, 5-HT3, and 5-HT6), adrenergic (α1), histaminic (H1), and muscarinic (M1, M2, M3, and M4) receptors. Olanzapine has a high affinity for the 5HT2A receptor, which is up to 5 times greater than the dopamine receptor, resulting in less propensity to the development of extrapyramidal side effects. The affinity of olanzapine for multiple receptors has lead to the identification of olanzapine as an important agent in the treatment of delirium, nausea, and vomiting. Olanzapine has been demonstrated to have opioid-sparing properties. Olanzapine is principally metabolized by glucuronidation, with a smaller metabolic contribution from the cytochrome oxidase system. Adverse effects of olanzapine include somnolence, postural hypotension, constipation, dizziness, restlessness, and weight gain. The purpose of this article is to outline the pharmacodynamics, pharmacology, and evidence for the use of olanzapine in palliative care.
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Martini, Michael L., Jing Liu, Caroline Ray, Xufen Yu, Xi-Ping Huang, Aarti Urs, Nikhil Urs, et al. "Defining Structure–Functional Selectivity Relationships (SFSR) for a Class of Non-Catechol Dopamine D1 Receptor Agonists." Journal of Medicinal Chemistry 62, no. 7 (March 15, 2019): 3753–72. http://dx.doi.org/10.1021/acs.jmedchem.9b00351.
Full textDissertations / Theses on the topic "D1-class receptor"
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Charrette, Andrew. "The Role of the Central Region of the Third Intracellular Loop of D1-Class Receptors in Signalling." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23080.
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The D1-class receptors (D1R, D5R) each possess distinct signaling characteristics; however, pharmacological selectivity between them remains elusive. The third intracellular loops (IL3) of D1R and D5R harbour divergent residues that may contribute to their individual signalling phenotypes. Here we probe the function of central region of IL3 of D1R and D5R using deletion mutagenesis. Radioligand binding and whole cell cAMP assays suggest that the N-terminal and C-terminal moieties of the central IL3 oppositely contribute to the constitutive and agonist-dependant activity of D1-Class receptors. Whereas the N-terminal deletions ablated constitutive activity and decreased DA-induced activation, C-terminal deletions induced robust increases. These data, interpreted in concert with structural predictions generated from homology modeling implicate the central IL3 as playing an important role in the activation and subtype-specific characteristics of the D1-class receptors. This study may serve as a basis for the development of novel drugs targeting the central IL3 region.
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Gower, Annette. "The Efficacy of Specific Activation of D1-class Dopamine Receptors to Enhance Motor Recovery in Mice Following Cortical Photothrombotic Stroke." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37619.
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Stroke is a widespread condition, which often leaves survivors with lasting deficits in motor function, however, physical rehabilitation is the only treatment available after the acute period. A large body of preclinical literature suggests dopamine-augmenting drugs, could enhance motor recovery following stroke. Unfortunately, mixed clinical results have prevented the implementation of such treatments, possibly due to the wide variety of G protein-coupled receptors these drugs can activate. Using a mouse photothrombosis stroke model and a battery of motor and sensorimotor behavioural tests, the current study aims to demonstrate proof of principle for the use of D1-class dopamine receptor agonists to enhance poststroke motor recovery and to evaluate the role of aerobic exercise rehabilitation in an asynchronous study design. The effect of light-dark cycle on behavioural outcome (horizontal ladder test, adhesive removal test, cylinder test) and histological outcome (infarct size) in photothrombotic stroke was evaluated in order to optimize the stroke model, but no there was no evidence of differences between strokes occurring during the light or dark period of a mouse’s circadian rhythm. A bioactive, suboptimal dose of D1-agonist dihydrexidine, was determined by evaluating its effect on locomotor activity and its ability to increase expression of immediate early gene c-fos. Using the determined dose, studies evaluating the efficacy of 7-days and 2-days of dihydrexidine administration on poststroke motor recovery, were performed, indicating efficacy of a 7-days, but not of a 2-days, course of treatment. The 7-days dihydrexidine treatment resulted in accelerated recovery as compared to a control group receiving saline. This work demonstrates, for the first time, proof of principle for the use of specific activation of D1-class dopamine receptors to enhance motor recovery following stroke.
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Zhang, Boyang. "Functional and Structural Insights into the First and Second Intracellular Domains for D1-Class Dopaminergic Receptors." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/35932.
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Previous studies have shown that the subtype-specific pharmacological properties of D1-class receptors (D1R and D5R) can be attributed to their third intracellular domain and C-terminal tail. However, the importance of their first and second intracellular domains (IC1 and IC2) has yet to be explored. Using mutagenesis and bioinformatics, we examine the functional and structural roles of Ser/Thr spanning IC1 and IC2—most of which are conserved not only among D1-class receptors but also among other GPCRs. Mutant receptors of human D1-class receptors (hD1R and hD5R) were constructed whereby all Ser and Thr were mutated to the respective Ala and Val in the IC1 region (termed ST1 mutant receptors) and in the IC2 region (termed ST2 mutant receptors). We found that hD1-ST2 and hD5-ST2 exhibited contrasting properties of agonist affinity, constitutive activity, and dopamine potency. On the other hand, both ST2 mutants underwent internalization as wild-type but displayed weakened desensitization abilities. Homology models, which have been refined under membrane simulations, illustrate that the conserved Ser3.55 and Thr3.65 utilize their side chains to anchor the loop regions of IC2 to cytoplasmic helices. We also found multiple functional alterations in the hD1-ST1 and hD5-ST2, but in a subtype-similar manner. Mutating the conserved Thr2.39 recapitulated the ablated basal activity and drastic decrease in dopamine potency previously witnessed in the hD1-ST1. Based on the recurring theme observed in crystal structures, the side-chain of Thr2.39 may help to position IC2 to have proper contacts with the G protein. Mutating the conserved Ser2.45 was found to be solely responsible for the elevated Emax (maximal response) of the hD1-ST1. Using single point mutagenesis, we further found that breaking the potential molecular interactions of Ser2.45 in hD1R (i.e. with Asn3.42 and Trp4.50) mimicked its elevated Emax. This elevated Emax was not found to be caused by altered abilities to undergo agonist-induced desensitization or internalization relative to hD1R. Overall, our work highlights the important functional and structural roles of IC1 and IC2 that needs to be accounted for in our current canonical models of GPCR signalling. Given the conserved nature of these Ser/Thr, our work may also be pertinent towards understanding the roles of IC1 and IC2 for other GPCRs.
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Albaker, Awatif. "Mutational Analysis to Define the Functional Role of the Third Intracellular Loop of D1-Class Dopaminergic Receptors." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/35063.
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The third intracellular loop (IL3) and cytoplasmic tail (CT), which are the most divergent regions between human D1-class dopaminergic receptors (hD1R and hD5R), have been implicated in modulating their subtype-specific functional phenotypes. The importance of the IL3 for Guanine nucleotide-binding protein (G-protein) coupling and specificity has long been acknowledged in the G-protein-coupled receptor (GPCR) field. However, the exact role the central region of the IL3, notably the N- and C-terminal moieties, plays in GPCR receptor functionality remains unclear. Studies in our laboratory indicated that the IL3/N-terminal moiety of hD1-class receptors appears to be critical for facilitating agonist-independent and dependent activation of hD1R and hD5R. Furthermore, the IL3/C-terminal portion of hD1-class receptors constrains the receptor in the inactive state and reduces receptor affinity for agonists and G-protein coupling. I put forward the following hypothesis: 1. The functional properties of hD1-class receptors are regulated via a molecular micro-switch present within the IL3 central region modulating the functional properties of the receptor distinctly, 2. The functional differences between D1R and D5R require structural elements from both N- and C-terminal halves of the IL3 central region, and 3. The molecular interplay between the N- and C-terminal halves of the IL3 central region is dependent on the amino acid chain length and content. Herein, I have employed site-directed mutagenesis, and alanine replacement approaches to analyze comprehensively the structural determinants within the N- and C-terminal moieties of the IL3 central region that regulate ligand binding and G-protein coupling properties of hD1-class receptors. Moreover, my Ph.D. research aimed to pinpoint whether the IL3 length and/or structural motif(s) regulate ligand binding and activation properties of hD1R and hD5R. The results of my study highlight the importance of structural elements from both the proximal and distal segments of the IL3/central region of hD1-class receptors for the ligand binding and receptor activation status. Additionally, my results underline the significance of preserving the length of the IL3 regardless of the amino acid content. This study also shows the pivotal role played by a phenylalanine residue, F2646.27, in the signaling properties of hD1R. Notably, mutating F2646.27 leads to a mutant hD1R with characteristics resembling those of constitutively active mutant GPCRs. Unraveling the amino acid/amino acids constraining the receptor in the inactive state will perhaps provide an attractive target for drug design. Future work aims at developing drugs that particularly bind to the intracellular face of hD1R and improving selectivity towards hD1R may prove useful in limiting the side effects associated with the conventional therapy of brain disorders such as in the case of L-DOPA induced dyskinesia (LID) seen in individuals suffering from Parkinson’s disease.
Book chapters on the topic "D1-class receptor"
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D. Maniero, Gregory. "Evolutionary Conservation of the Role of CD4 as a Receptor for Interleukin-16." In Interleukins - The Immune and Non-Immune Systems’ Related Cytokines. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96951.
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The interaction of CD4 with MHC class II during helper T-cell activation and effector function is required for the initiation of an adaptive immune response in all gnathostomes. CD4 is comprised of four immunoglobulin domains but most likely arose from an ancestral two-domain homolog. The distal, D1 domain of CD4 binds to non-polymorphic regions of the MHC molecule, but despite the absolute requirement for this interaction, the sequence and structure of this domain are not well conserved through phylogeny. Conversely, the proximal, D4 domain of CD4 contains the binding site of the cytokine IL-16 and is highly conserved in its amino acid structure. IL-16 is a cytokine that has been described in a wide variety of invertebrate and vertebrate species. The CD4-binding residues on IL-16 are highly conserved throughout phylogeny, allowing for promiscuous binding of IL-16 to CD4 between members of unrelated taxa. This chapter aims to present structural, and functional support for the hypothesis that the CD4 co-receptor of the TCR arose from a primordial receptor for IL-16.