Relevant bibliographies by topics / Dopamine type I receptor

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Academic literature on the topic 'Dopamine type I receptor'

Author: Grafiati
Published: 19 October 2024

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Journal articles on the topic "Dopamine type I receptor"

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Shariati, G. H., G. Ahangari, M. R. Asadi, F. Poyafard, and H. R. Ahmadkhaniha. "Dopamine Receptor Gene Expression Changes in Peripheral Blood Mononuclear Cells from Schizophrenic Patients Treated with Haloperidol and Olanzapine." European Journal of Inflammation 7, no. 2 (May 2009): 71–76. http://dx.doi.org/10.1177/1721727x0900700203.

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We investigated dopamine receptor gene expression in peripheral blood mononuclear cells of schizophrenic patients before and after treatment. Also dopamine receptor genes expression profile was compared in two treatment groups including haloperidol and olanzapine. The peripheral blood mononuclear cells were separated from whole blood by Ficoll-hypaque; the total cellular RNA was extracted and the cDNA was synthesized. This process was followed by real-time polymerase chain reaction 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 in lymphocytes. Dopamine receptor gene expression profile in dopamine receptor D2 gene and dopamine receptor D4 gene showed significant changes that were correlated with the type of treatment and Clinical Global Impressions score improvement. In conclusion, the present study shows that human lymphocytes express dopamine receptor D1–D5 genes. Moreover, investigated dopamine receptors gene expression in peripheral blood mononuclear cells of schizophrenic patients correlated with clinical symptom improvement.
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Sarkar, D. K., K. Chaturvedi, S. Oomizu, N. I. Boyadjieva, and C. P. Chen. "Dopamine, Dopamine D2 Receptor Short Isoform, Transforming Growth Factor (TGF)-β1, and TGF-β Type II Receptor Interact to Inhibit the Growth of Pituitary Lactotropes." Endocrinology 146, no. 10 (October 1, 2005): 4179–88. http://dx.doi.org/10.1210/en.2005-0430.

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The neurotransmitter dopamine is known to inhibit prolactin secretion and the proliferation of lactotropes in the pituitary gland. In this study, we determined whether dopamine and TGFβ1 interact to regulate lactotropic cell proliferation. We found that dopamine and the dopamine agonist bromocriptine stimulated TGFβ1 secretion and TGFβ1 mRNA expression but inhibited lactotropic cell proliferation both in vivo and in vitro. The dopamine’s inhibitory action on lactotropic cell proliferation was blocked by a TGFβ1-neutralizing antibody. We also found that PR1 cells, which express low amounts of the dopamine D2 receptor, demonstrated reduced expression of TGFβ1 type II receptor and TGFβ1 mRNA levels and had undetectable levels of TGFβ1 protein. These cells showed a reduced TGFβ1 growth-inhibitory response. Constitutive expression of the D2 receptor short isoform, but not the D2 receptor long isoform, induced TGFβ1 and TGFβ1 type II receptor gene expression and recovered dopamine- and TGFβ1-induced growth inhibition in PR1 cells. The constitutive expression of D2 receptor short isoform also reduced the tumor cell growth rate. These data suggest that a TGFβ1 system may mediate, in part, the growth-inhibitory action of dopamine on lactotropes.
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Peiser, Christian, Marcello Trevisani, David A. Groneberg, Q. Thai Dinh, Doerthe Lencer, Silvia Amadesi, Barbara Maggiore, Selena Harrison, Pierangelo Geppetti, and Axel Fischer. "Dopamine type 2 receptor expression and function in rodent sensory neurons projecting to the airways." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 1 (July 2005): L153—L158. http://dx.doi.org/10.1152/ajplung.00222.2004.

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Agonists of the dopamine receptors have been demonstrated to have bronchodilatory properties in pathologically constricted airways. The mechanism by which these agonists induce bronchodilatation is thought to involve airway sensory nerves. In this study, the expression and function of dopamine D2 receptor were examined in sensory ganglia supplying the airways. Neuronal dopamine D2 receptor mRNA expression was demonstrated by single-cell RT-PCR following laser-assisted microdissection. The projection of the neurons to the airways was confirmed by retrograde neuronal labeling. In functional studies, dopamine D2 receptor agonists (AR-C65116AB and ropinirole) inhibited intraneuronal calcium mobilization in rat capsaicin-sensitive primary sensory neurons and capsaicin-induced plasma extravasation in the rat trachea. Our results provide support to the hypothesis that dopamine D2 receptor activation inhibits neurogenic inflammation and proinflammatory reflex responses.
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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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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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Ding, Guoliang, Rob F. Wiegerinck, Ming Shen, Anca Cojoc, Carlo M. Zeidenweber, and Mary B. Wagner. "Dopamine increases L-type calcium current more in newborn than adult rabbit cardiomyocytes via D1 and β2 receptors." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 5 (May 2008): H2327—H2335. http://dx.doi.org/10.1152/ajpheart.00993.2007.

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Dopamine is used to treat heart failure, particularly after cardiac surgery in infants, but the mechanisms of action are unclear. We investigated differences in the effect of dopamine on L-type calcium current ( ICa) between newborn (NB, 1–4 days) and adult (AD, 3–4 mo) rabbit ventricular myocytes. Myocytes were enzymatically dissociated from NB and AD rabbit hearts. ICa was recorded by using the whole cell patch-clamp technique. mRNA levels of cardiac dopamine receptor type 1 (D1), type 2 (D2), and β-adrenergic receptors (β-ARs) were measured by real-time RT-PCR. Dopamine (100 μM) increased ICa more in NB (Emax 87 ± 10%) than in AD ventricular cells (Emax 21 ± 3%). Further investigation of this difference showed that mRNA levels of the D1 receptor were significantly higher in NB, and, with β-AR blockade, dopamine increased ICa more in NB than AD cells. Additionally, SKF-38393 (selective D1 receptor agonist) significantly increased ICa by 55 ± 4% in NB ( P < 0.05, n = 4) and by 11 ± 1% in AD ( P < 0.05, n = 6). Dopamine in the presence of SCH-23390 (D1 receptor antagonist) increased ICa in NB cells by 67 ± 5% and by 22 ± 2% in AD cells, suggesting a role for β-AR stimulation. Selective blockade of β1- or β2-receptors (with block of D1 receptors) showed that the β-AR action of dopamine in the NB was largely mediated via β2-AR activation. Dopamine produces a larger increase in ICa in NB cardiomyocytes compared with ADs. The mechanism of action is not only through β2-ARs but also due to higher expression of cardiac D1 receptor in NB.
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MORA-FERRER, CARLOS, and VOLKER GANGLUFF. "D2-dopamine receptor blockade impairs motion detection in goldfish." Visual Neuroscience 17, no. 2 (March 2000): 177–86. http://dx.doi.org/10.1017/s0952523800171196.

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Under photopic illumination conditions, motion detection in goldfish is dominated by the long-wavelength-sensitive cone type (L-cone), and under scotopic conditions motion it is determined by rods (Schaerer & Neumeyer, 1996). The switch from rod-dominated to cone-dominated motion detection occurs during light adaptation. It has been suggested that dopamine acts as a neuronal light-adaptative signal. It is known that dopamine affects wavelength discrimination through D1-dopamine receptors (Mora-Ferrer & Neumeyer, 1996), and the dorsal light reflex through D1- and D2-dopamine receptors (Lin & Yazulla, 1994a). The purpose of this study was to determine whether dopamine influenced movement detection by goldfish, and if so, which dopamine receptor was involved. The D2-dopamine receptor antagonist sulpiride reduced the animal's sensitivity to the moving stimulus, whereas SCH 23390, a D1-dopamine receptor antagonist, did not have any effect. The effect of sulpiride is discussed in relation to known sulpiride effects on retinal neurons and the retinal pigment epithelium.
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Hayashida, Yuki, and Andrew T. Ishida. "Dopamine Receptor Activation Can Reduce Voltage-Gated Na+ Current by Modulating Both Entry Into and Recovery From Inactivation." Journal of Neurophysiology 92, no. 5 (November 2004): 3134–41. http://dx.doi.org/10.1152/jn.00526.2004.

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We tested whether dopamine receptor activation modulates the voltage-gated Na+ current of goldfish retinal ganglion cells, using a fast voltage-clamp amplifier, perforated-patch whole cell mode, and a physiological extracellular Na+ concentration. As found in other cells, activators of D1-type dopamine receptors and of protein kinase A reduced the amplitude of current activated by depolarizations from resting potential without altering the current kinetics or activation range. However, D1-type dopamine receptor activation also accelerated the rate of entry into inactivation during subthreshold depolarizations and slowed the rate of recovery from inactivation after single, brief depolarizations. Our results provide the first evidence in any preparation that D1-type receptor activation can produce both of these latter effects.
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Pfeiffer-Linn, C., and E. M. Lasater. "Dopamine modulates in a differential fashion T- and L-type calcium currents in bass retinal horizontal cells." Journal of General Physiology 102, no. 2 (August 1, 1993): 277–94. http://dx.doi.org/10.1085/jgp.102.2.277.

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White bass (Roccus chrysops) retinal horizontal cells possess two types of voltage-activated calcium currents which have recently been characterized with regard to their voltage dependence and pharmacology (Sullivan, J., and E. M. Lasater. 1992. Journal of General Physiology. 99:85-107). A low voltage-activated transient current was identified which resembles the T-type calcium current described in a number of other preparations, along with a sustained high threshold, long-lasting calcium current that resembles the L-type calcium current. Here we report on the modulation of horizontal cell calcium channels by dopamine. Under whole-cell voltage clamp conditions favoring the expression of both calcium currents, dopamine had opposing actions on the two types of voltage-sensitive calcium currents in the same cone-type horizontal cell. The L-type calcium current was significantly potentiated by dopamine while the T-type current was simultaneously reduced. Dopamine had no effect on calcium currents in rod-type horizontal cells. Both of dopamine's actions were mimicked with the D1 receptor agonist, SKF 38393, and blocked by application of the D1 specific antagonist, SCH 23390. Dopamine's actions on the two types of calcium currents in white bass horizontal cells are mimicked by the cell membrane-permeant cyclic AMP derivative, 8-(4-chlorophenylthio)-cyclic AMP, suggesting that dopamine's action is linked to a cAMP-mediated second messenger system. Furthermore, the inhibitor of cAMP-dependent protein kinase blocked both of dopamine's actions on the voltage-dependent calcium channels when introduced through the patch pipette. This indicates that protein phosphorylation is involved in modulating horizontal cell calcium channels by dopamine. Taken together, these results show that dopamine has differential effects on the voltage-dependent calcium currents in retinal horizontal cells. The modulation of these currents may play a role in shaping the response properties of horizontal cells.
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Milienne-Petiot, Morgane, Lucianne Groenink, Arpi Minassian, and Jared W. Young. "Blockade of dopamine D1-family receptors attenuates the mania-like hyperactive, risk-preferring, and high motivation behavioral profile of mice with low dopamine transporter levels." Journal of Psychopharmacology 31, no. 10 (September 27, 2017): 1334–46. http://dx.doi.org/10.1177/0269881117731162.

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Background: Patients with bipolar disorder mania exhibit poor cognition, impulsivity, risk-taking, and goal-directed activity that negatively impact their quality of life. To date, existing treatments for bipolar disorder do not adequately remediate cognitive dysfunction. Reducing dopamine transporter expression recreates many bipolar disorder mania-relevant behaviors (i.e. hyperactivity and risk-taking). The current study investigated whether dopamine D1-family receptor blockade would attenuate the risk-taking, hypermotivation, and hyperactivity of dopamine transporter knockdown mice. Methods: Dopamine transporter knockdown and wild-type littermate mice were tested in mouse versions of the Iowa Gambling Task (risk-taking), Progressive Ratio Breakpoint Test (effortful motivation), and Behavioral Pattern Monitor (activity). Prior to testing, the mice were treated with the dopamine D1-family receptor antagonist SCH 23390 hydrochloride (0.03, 0.1, or 0.3 mg/kg), or vehicle. Results: Dopamine transporter knockdown mice exhibited hyperactivity and hyperexploration, hypermotivation, and risk-taking preference compared with wild-type littermates. SCH 23390 hydrochloride treatment decreased premature responding in dopamine transporter knockdown mice and attenuated their hypermotivation. SCH 23390 hydrochloride flattened the safe/risk preference, while reducing activity and exploratory levels of both genotypes similarly. Conclusions: Dopamine transporter knockdown mice exhibited mania-relevant behavior compared to wild-type mice. Systemic dopamine D1-family receptor antagonism attenuated these behaviors in dopamine transporter knockdown, but not all effects were specific to only the knockdown mice. The normalization of behavior via blockade of dopamine D1-family receptors supports the hypothesis that D1 and/or D5 receptors could contribute to the mania-relevant behaviors of dopamine transporter knockdown mice.
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Dissertations / Theses on the topic "Dopamine type I receptor"

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Hatcher-Solis, Candice N. "PHARMACOLOGICAL IMPLICATIONS OF ADENOSINE 2A RECEPTOR- DOPAMINE TYPE 2 RECEPTOR HETEROMERIZATION." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4458.

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G protein-coupled receptors (GPCRs) are heptahelical, transmembrane proteins that mediate a plethora of physiological functions by binding ligands and releasing G proteins that interact with downstream effectors. GPCRs signal as monomers, complexes of the same receptor subtype (homomers), or complexes of different receptor subtypes (heteromers). Recently, heteromeric GPCR complexes have become attractive targets for drug development since they exhibit distinct signaling and cell-specific localization from their homomeric counterparts. Yet, the effect of heteromerization on the pharmacology of many GPCR homomers remains unknown. Therefore, we have undertaken the task to examine the effect of heteromerization on Gs signaling through the adenosine 2A receptor (A2AR) and Gi signaling through the dopamine type 2 receptor (D2R) since the A2AR-D2R heteromer is an emerging therapeutic target for Parkinson’s disease (PD). We examined the effect of heteromerization on A2AR and D2R homomeric signaling using electrophysiology and the Xenopus laevis oocyte heterologous expression system. G protein-coupled inwardly rectifying potassium channels (GIRKs) were used as reporters for Gi signaling because activation leads to direct Gbeta-gamma (Gβγ)-mediated stimulation of the GIRK current. We also coupled GIRK channels to Gs signaling by overexpressing Gαs and signaling throughGαsβγ. Our electrophysiological assay is innovative because it allows us to optimize the conditions of heteromerization and directly observe GPCR signaling at the G protein level. Our data demonstrate that heteromer formation alone decreases dopamine-elicited Gi signaling through the D2R and CGS-21680-elicited Gs signaling through the A2AR. Furthermore, this reciprocal antagonism was predominately due to changes in efficacy versus potency. We also examined crosstalk observing that applying agonists or antagonists to the adjacent receptor further modulate this inhibition with the combination of agonists and antagonists relieving inhibition. Mutating the A2AR-D2R heteromer interface abrogated all of the aforementioned ligand-induced effects on G protein signaling through the A2AR-D2R heteromer. We are currently aiming to validate our results from the oocyte experiments with an in vivo model. Our data further elucidate the effect of various ligands on G protein signaling through the A2AR- D2R heteromer, which may facilitate future studies that examine A2AR-D2R heteromer signaling.
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ZANINOVICH, OREL ANTHONY. "THE CLONING OF AN INDR-TYPE DOPAMINE RECEPTOR IN MANDUCA SEXTA." Thesis, The University of Arizona, 2008. http://hdl.handle.net/10150/192256.

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Mann, Miranda Jane. "A neuropsychological investigation of dopamine receptor 4 differences among attention deficit hyperactivity disorder-combined type and control children /." Digital version accessible at:, 2000. http://wwwlib.umi.com/cr/utexas/main.

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Gorji, Hassan. "Role of adenylyl cyclase type 5 in the regulation of the dopamine D3 receptor phosphorylation." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/27364.

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Adenylyl cyclase type 5 (AC5) is expressed in the brain where the highest density of the dopamine D3 receptor (D3R) has been found. The D3R-mediated Gi/o protein activation leads to a specific inhibition of AC5. Therefore, as AC5 is the main signalosome partner of D3R, I hypothesize that D3R phosphorylation is differentially regulated in cells expressing AC5. In HEK293 cells expressing D3R alone, D3R undergo dopamine-induced phosphorylation. Interestingly, in cells co-expressing AC5 and D3R, D3R undergoes a Galphai-dependent dephosphorylation upon dopamine exposure while retaining its ability to be phosphorylated in a Src-dependent manner under basal conditions. In cells co-expressing D3R and AC5, dopamine-induced D3R dephosphorylation and Gi/o mediated inhibition of cAMP production are specifically blocked by pharmacological inhibitors of the serine/threonine phosphatase PP2B and tyrosine phosphatases. Overall, our results suggest a novel paradigm in G protein-coupled receptor signaling whereby AC5 serves as a potential scaffolding complex containing phosphatases regulating the D3R phosphorylation status.
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Maier, Annette Louise. "Comparative regional ontogeny of dopamine D₁ receptor binding and mRNA expression in pre- and postnatal rat brain /." Zürich, 1994. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10902.

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Etchepare, Laetitia. "Role of glutamate N-Methyl-D-Aspartate receptor surface trafficking in the firing pattern of midbrain dopaminergic neurons." Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0849/document.

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Les neurones dopaminergiques (DA) mésencéphaliques jouent un rôle prépondérant dans de nombreuses fonctions cérébrales telles que la motivation, mais ils sont également impliques dans l’émergence de pathologies telles que la maladie de Parkinson et l’addiction aux drogues. Ces processus ayant en commun de modifier l’activité de décharge des neurones DA mésencéphaliques, il est d’une importance primordiale de comprendre les mécanismes sous-tendant cette activité. Parmi les différents canaux ioniques et récepteurs impliques dans la génération de l’activité de décharge des neurones DA, les récepteurs au glutamate de type N-Methyl-D-Aspartate (NMDAR) et les canaux potassiques calcium-dépendants SK régulent fortement le patron de décharge, et interagissent fonctionnellement dans divers types neuronaux incluant les neurones DA. Cependant, les mécanismes mis en jeu dans cette régulation restent méconnus. Le couplage fonctionnel des NMDAR et des canaux SK dépendant notamment de leur distribution membranaire relative, nous avons émis l’hypothèse que la diffusion latérale des NMDAR, processus qui régule la localisation de surface du récepteur, pouvait jouer un rôle dans le patron de décharge des neurones DA via la modulation de la fonction des canaux SK. Nous avons tout d’abord montre que les NMDAR membranaires étaient mobiles dans les neurones DA en culture. L’altération de leur trafic de surface par immobilisation avec des anticorps anti-NMDAR modifie profondément la régularité du patron de décharge des neurones DA issus de tranches aigües de mésencéphale, alors que le blocage pharmacologique des NMDAR est sans effet. De plus, j’ai mis en évidence qu’un bloqueur des canaux SK, l’apamine, qui induit un changement similaire de la regularite du patron de décharge en condition contrôle, etait moins efficace lorsque la mobilité latérale des NMDAR etait alteree. Ainsi, ces résultats démontrent que la dynamique de surface des NMDAR module le patron de décharge des neurones DA en régulant la fonction des canaux SK
Midbrain dopaminergic (DA) neurons play several key functions in the brain such as the processing of salient information but are also associated with the emergence of pathologies including Parkinson’s disease and drug addiction. Because these processes have in common to modify the firing activity of midbrain DA neurons, it is of crucial importance to understand the mechanisms underlying this activity. Among the various ions channels and receptors involved in the generation of the firing activity of midbrain DA neurons, glutamate N-methyl-D-aspartate receptors (NMDAR) and calciumdependent potassium SK channels strongly modulate the firing pattern and functionally interact in several neuronal types including DA neurons. However, the mechanisms by which they regulate the firing pattern are poorly understood. Since the functional coupling between NMDAR and SK channels depends on their relative membrane distribution, we hypothesized that the lateral diffusion of NMDAR, which regulates the surface localization of the receptor, could play a role in the firing pattern of midbrain DA neurons through the modulation of SK channel function. We showed first that membrane NMDAR was highly mobile in cultured DA neurons. Alteration of its surface trafficking by a crosslink with NMDAR antibodies profoundly modified the regularity of the firing pattern of DA neurons in midbrain slices, whereas pharmacological blockade of NMDAR did not affect it. Furthermore, a SK channel blocker, which induces a similar change in the firing regularity in control conditions, was less effective when NMDAR surface trafficking was altered. Taken together, these results demonstrate that NMDAR surface dynamics modulate the firing pattern of midbrain DA neurons by regulating SK channel function
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Roberts-Crowley, Mandy L. "Modulation of Cav1.3 L-Type Calcium Channels by Arachidonic Acid and Muscarinic M1 Receptors: A Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/348.

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Membrane excitability, gene expression, and neurotransmitter release are all controlled by voltage-gated L-type Ca2+ (L- )channels. In turn, Ca2+ channels are highly regulated by signal transduction cascades initiated by G protein-coupled receptor (GPCR) activation. In medium spiny neurons of the striatum, both the muscarinic M1 receptors (M1R) and dopaminergic D2 receptors (D2R) specifically inhibit the Cav1.3 L-channel. In Chapters III and IV, the pathways downstream of M1Rs and D2Rs are examined to determine whether an overlap or intersection in inhibition of Cav1.3 occurs by these two receptors. Transient transfection of Cav1.3 channels in HEK 293 cells, stably transfected with the M1R, and in ST14A cells were used as model systems. While a further characterization of ST14A cells determined that they exhibit a striatal profile, D2Rs or M1Rs did not inhibit Cav1.3. Lack of current inhibition may be due to the finding of no detectable expression of phospholipase Cβ-1 protein in ST14A cells. Ca2+ channels are multiprotein complexes comprised of α1, β, and α2δ subunits. While the actions of arachidonic acid (AA) have been shown to mimic M1R inhibition of L-current in superior cervical ganglion neurons, the precise identity of the L-channel in these neurons -either Cav1.2 or Cav1.3 or both- is not known. The transfected model systems allowed for the analysis of whole-cells currents with different β subunit combinations as well as the study of only Cav1.3 channels. In Chapter III, I show that activation of M1Rs with the agonist Oxo-M inhibited Cav1.3 channels coexpressed with either β1b, β2a, β3, or β4 subunits. Surprisingly, the magnitude of Cav1.3, β2a currents was inhibited less than Cav1.3 currents with other β subunits. In Chapter V, AA is shown to mimic the profile of M1R stimulation on Cav1.3 currents. The magnitude of Cav1.3, β2a currents was inhibited less than Cav1.3 currents with other β subunits by AA. This discovery points to a novel role for accessory β subunits in altering the magnitude of AA inhibition and kinetic changes of Cav1.3. Arachidonic acid (AA) inhibits Ca2+ channels by an unknown mechanism at an unknown site. In Chapter V, I found that Cavl.3 inhibition by AA was state-dependent and most likely stabilizes a closed channel conformation. The finding that the Ca2+ channel accessory β subunit alters the magnitude of AA inhibition and kinetic changes of Cav1.3 suggests that AA could alter processes which rely on L-channels such as Ca2+-dependent gene expression, secretion and membrane excitability.
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Lucas, Guillaume. "Etude in vivo des modalités d'intervention de la sérotonine et des récepteurs sérotoninergiques de type 5-HT/2A/2C, 5-HT3 et 5-HT4 dans le contrôle de la transmission dopaminergique nigro-striée et mésoaccumbale chez le rat." Bordeaux 2, 1999. http://www.theses.fr/1999BOR28692.

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Hegron, Alan. "Implication des récepteurs de la mélatonine dans les troubles neurologiques et le diabète de type 2 et identification de régions clés du récepteur MT1 responsables de sa sélectivité fonctionnelle." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS555/document.

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La mélatonine est une neurohormone produite principalement par la glande pinéale de manière circadienne et agissant par l’activation de deux récepteurs couplés aux protéines G (RCPGs) appelés MT1 et MT2. La mélatonine régule de nombreuses fonctions physiologiques importantes. La régulation des niveaux de dopamine (DA) et de glucose en font partie mais nous ne savons pas clairement comment la mélatonine les régule.Les niveaux de DA extracellulaire sont principalement régulés par son transporteur (DAT) responsable de sa recapture dans les neurones présynaptiques afin de prévenir d’une hyperactivation des récepteurs dopaminergiques. Par conséquent, nous avons vérifié le rôle de DAT dans la régulation du système dopaminergique par le système mélatoninergique. Nous avons montré qu’en interagissant avec la forme immature non-glycosylée de DAT, MT1 et MT2 le retiennent dans le réticulum endoplasmique régulant ainsi son expression à la surface cellulaire et donc la recapture de la DA. De la même manière, les souris déficientes en MT1 ou MT2 ont montré une augmentation de la recapture de la DA dans les synaptosomes de striatum et une baisse de l’hypermotilité induite par l’amphétamine. Dans ce projet nous avons ainsi révélé un nouveau lien entre les systèmes mélatoninergiques et dopaminergiques basé sur la formation de complexes moléculaires entre les récepteurs de la mélatonine et DAT.Afin de mieux comprendre le rôle de la mélatonine dans la régulation des niveaux de glucose, nous avons ensuite étudié l’implication de variants génétiques de MT2 dans le développement du diabète de type 2 (DT2). Des études antérieures avaient montré que des variants naturels défectueux fonctionnellement étaient associés à un risque de développer le DT2. Afin de déterminer plus précisément les propriétés défectueuses en lien avec le DT2, nous avons mesuré l’activation spontanée et celle induite par la mélatonine de 40 variants MT2. Nous avons ainsi montré que des défauts d’activation des protéines Gαi et Gαz induite par la mélatonine et de recrutement spontané de la βarrestine-2 sont significativement reliés à un risque de développer le DT2. Les résultats expérimentaux corrélaient avec les prédictions de l’analyse sur le score d’évolution. Ce travail permettra de nouvelles avancées dans la recherche de traitements personnalisés pour les personnes portants les mutations sur MT2 afin qu’il retrouve une réponse non défectueuse.Le séquençage de 9393 personnes a permis l’identification de 32 variants naturels MT1. Le récepteur MT1 sauvage et les variants ont ainsi été caractérisés grâce aux techniques de transfert d’énergie par résonnance de bioluminescence (BRET). Nous avons montré que MT1 active les protéines Gαi/o, Gα12 et Gα15 et recrute la βarrestine-2. L’analyse des résultats par factorisation matricielle non linéaire a révélé l’existence de 5 clusters caractérisés par différents profils de signalisation. La modélisation 3D par homologie de MT1 a permis de déterminer l’impact de chaque variant sur l’activation du récepteur et ses interactions avec les protéines G et la βarrestine-2. Ce projet a ainsi permis de démontrer que des variants naturels sont très intéressant afin de comprendre les mécanismes d’action des RCPGs. En résumé, ce travail contribue à la compréhension des fonctions des récepteurs à la mélatonine et souligne leur importance dans la régulation du système dopaminergique et de l’homéostasie glucidique. Nos résultats offrent de nouvelles perspectives dans la recherche de nouveaux traitements personnalisés pour les patients souffrant d’un dérèglement du système dopaminergique ou de DT2
Melatonin is a neurohormone mainly released from the pineal gland in a circadian manner acting through two G protein-coupled receptors (GPCRs) called MT1 and MT2. Melatonin regulates many important physiological functions. Regulation of dopamine (DA) and glucose levels are two of them but how they do this is not clear.Extracellular DA levels are mainly regulated by its transporter (DAT) which mediates DA re-uptake into presynaptic nerve termini to prevent DA receptor hyperactivation in the presynaptic cleft. Consequently, we verified the role of DAT in the regulation of the DA system by melatonin. We showed that MT1 and MT2, by interacting with the immature non-glycosylated form of DAT retain DAT in the endoplasmic reticulum thus regulating DAT cell surface expression and DA reuptake. Consistently, mice with targeted deletion of MT1 and MT2 show markedly enhanced DA uptake in striatal synaptosomes and decreased amphetamine-induced locomotor activity. Collectively, we revealed here a molecular link between the melatonin and DA systems, which is based on the formation of a molecular complex between melatonin receptors and DAT.To better understand the role of melatonin on the regulation of glucose levels, we studied the involvement of genetic variants of MT2 in the development of type 2 diabetes (T2D). Previous studies showed that natural loss-of-function variants of MT2 associate with T2D risk. To determine more precisely the defective properties linked to T2D risk we monitored spontaneous and melatonin-induced activation of different signaling pathways by 40 MT2 variants. We show that defects in melatonin-induced Gαi and Gαz activation and spontaneous βarrestin-2 recruitment are most significantly associated to T2D risk. Experimental results correlated well with those predicted by evolutionary lineage analysis. This work will help to propose personalized treatments for MT2 variant carriers to recover their defective responses.Sequencing of 9393 individuals resulted in the identification of 32 natural MT1 variants. MT1 wild-type and variants were functionally characterized in bioluminescence resonance energy transfer (BRET) assays. We showed that MT1 activates Gαi/o, Gα12 and Gα15 proteins and recruits βarrestin-2. Analyzes of results by non-linear matrix factorization revealed the existence of 5 clusters characterized by different signaling profiles. Computational homology modeling of the 3D model of MT1 helped to determine the impact of each variant on receptor activation and interaction with G proteins and βarrestin-2. Collectively, our data illustrate that natural variants are powerful tools to understand the molecular basis of GPCR function. Overall, this work contributes to our understanding of the function of melatonin receptors and highlights their importance in the regulation of the DA system and glucose homeostasis. Our results will open new, personalized therapeutic options for patient suffering from a defective DA system or T2D
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Thirtamara, Rajamani Keerthi Krishnan. "Animal Models of Drug Addiction and Autism Spectrum Disorders." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1386011455.

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Books on the topic "Dopamine type I receptor"

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Tupala, Erkki. Dopamine receptors and transporters in type 1 and 2 alcoholism measured with postmortem human whole hemisphere autoradiography. Kuopio: University of Kuopio, 2001.

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Tiberi, Mario. Dopamine receptor technologies. New York, NY: Humana Press, 2015.

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Tiberi, Mario, ed. Dopamine Receptor Technologies. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2196-6.

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Donthamsetti, Prashant Chandra. Dissecting Dopamine D2 Receptor Signaling. [New York, N.Y.?]: [publisher not identified], 2015.

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L, Waddington John, ed. D1:D2 dopamine receptor interactions. London: Academic Press, 1993.

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Boileau, Isabelle, and Ginetta Collo, eds. Therapeutic Applications of Dopamine D3 Receptor Function. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23058-5.

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Knapp, Mark. Development of dopamine receptor expressing adenoviral vectors. Ottawa: National Library of Canada, 1997.

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R, Demirdamar, and Jenner Peter 1946-, eds. Dopamine receptor subtypes: From basic science to clinical application. Amsterdam: IOS Press, 1998.

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Ray, Avi Andrew. SH3 binding domains in the dopamine D(3) receptor. Ottawa: National Library of Canada, 1999.

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Zawarynski, Paul. Dopamine D2 receptor monomers, dimers and higher order oligomers. Ottawa: National Library of Canada, 1998.

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Book chapters on the topic "Dopamine type I receptor"

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Turco, Raymond. "Dopamine Receptor." In Encyclopedia of Animal Cognition and Behavior, 1–5. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47829-6_1256-1.

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Turco, Raymond. "Dopamine Receptor." In Encyclopedia of Animal Cognition and Behavior, 2120–25. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-55065-7_1256.

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Fuxe, Kjell, Daniel Marcellino, Diego Guidolin, Amina Woods, and Luigi Agnati. "Dopamine Receptor Oligomerization." In The Dopamine Receptors, 255–80. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-333-6_10.

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Hazelwood, Lisa A., R. Benjamin Free, and David R. Sibley. "Dopamine Receptor-Interacting Proteins." In The Dopamine Receptors, 219–54. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-333-6_9.

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Deth, Richard C. "The Dopamine D4 Receptor." In Molecular Origins of Human Attention, 23–36. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0335-4_4.

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Richtand, Neil M., Laurel M. Pritchard, and Lique M. Coolen. "Dopamine Receptor Alternative Splicing." In Dopamine and Glutamate in Psychiatric Disorders, 45–61. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1007/978-1-59259-852-6_2.

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Civelli, Olivier, James Bunzow, Paul Albert, Hubert H. M. Van Tol, and David Grandy. "The Dopamine D2 Receptor." In Molecular Biology of G-Protein-Coupled Receptors, 160–69. Boston, MA: Birkhäuser Boston, 1992. http://dx.doi.org/10.1007/978-1-4684-6772-7_7.

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Cepeda, Carlos, Véronique M. André, Emily L. Jocoy, and Michael S. Levine. "Dopamine Receptor Modulation of Glutamatergic Neurotransmission." In The Dopamine Receptors, 281–302. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-333-6_11.

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Lee, Frankie H. F., and Albert H. C. Wong. "Dopamine Receptor Genetics in Neuropsychiatric Disorders." In The Dopamine Receptors, 585–632. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-333-6_19.

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Moreira, Irina S., Lei Shi, Zachary Freyberg, Spencer S. Ericksen, Harel Weinstein, and Jonathan A. Javitch. "Structural Basis of Dopamine Receptor Activation." In The Dopamine Receptors, 47–73. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-333-6_3.

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Conference papers on the topic "Dopamine type I receptor"

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Kamasak, Mustafa E., Charles A. Bouman, Bradley T. Christian, and Evan D. Morris. "Imaging D2-Dopamine Receptor using PET." In 2007 IEEE 15th Signal Processing and Communications Applications. IEEE, 2007. http://dx.doi.org/10.1109/siu.2007.4298698.

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Moritz, Amy E., Nora S. Madaras, Kirsten K. Snyder, Noelia M. Boldizsar, Raphael Haider, Julia Drube, Arun K. Ghosh, John JG Tesmer, Carsten Hoffmann, and David R. Sibley. "Regulation of Dopamine Receptor Subtypes by G Protein-Coupled Receptor Kinase Isoforms." In ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.159.988010.

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Liu, X., J. Guan, F. Tao, and B. Mao. "Acupuncture Zusanli Regulate COPD Inflammation Through Dopamine D2 Receptor." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4755.

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Harrison, J. M., I. Nir, M. Rubinstein, M. J. Low, D. K. Grandy, and P. M. Iuvone. "Retinal Function in Dopamine D4 Receptor Knockout (D4KO) Mice." In Vision Science and its Applications. Washington, D.C.: OSA, 2000. http://dx.doi.org/10.1364/vsia.2000.fd2.

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Javadi, Arman, Nicholas Forsythe, Alaa Refaat, Jessica-Ann Weir, Hajrah Khawaja, David Waugh, Rohinton Tarapore, Joshua E. Allen, Patrick Johnston, and Sandra Van Schaeybroeck. "Abstract 3448: Targeting the dopamine receptor 2 inBRAFmutant colorectal cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3448.

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Uysal, Mehmet Atilla, Ulgen Sever, and Sacide Pehlivan. "The dopamine receptor D4 VNTR 48bp gene variant in nicotine addiction." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa1486.

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Raghuraman, Gayatri, Nanduri R. Prabhakar, and Ganesh K. Kumar. "Dopamine D1 Receptor Signaling Mediates Altered GABA Synthesis By Intermittent Hypoxia." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6630.

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Blake, Keyana, Basant Hens, and Anthony J. Baucum. "Investigating the role of spinophilin in mediating Dopamine D2 Receptor Activity." In ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.321.940880.

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Wen, Ruojian, Xiaoqing Chen, Dan Huang, Minjie Chen, and Yuwei Liu. "Sleep Deprivation Increased Dopamine D2 Receptor Expression through Downregulation of miR-9." In 2015 7th International Conference on Information Technology in Medicine and Education (ITME). IEEE, 2015. http://dx.doi.org/10.1109/itme.2015.122.

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Madaras, Nora S., Michele L. Rankin, R. Benjamin Free, Raphael Haider, Julia Drube, Arun K. Ghosh, John JG Tesmer, Carsten Hoffmann, David R. Sibley, and Amy E. Moritz. "Delineation of the G Protein-Coupled Receptor Kinase Phosphorylation Sites Within the D1 Dopamine Receptor and Their Role in Regulating Receptor Function." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.154110.

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Reports on the topic "Dopamine type I receptor"

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Dr. Jogeshwar Mukherjee. Development of dopamine receptor radiopharmaceuticals for the study of neurological and psychiatric disorders. Office of Scientific and Technical Information (OSTI), January 2009. http://dx.doi.org/10.2172/944919.

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Mukherjee, J. Development of dopamine receptor radiopharmaceuticals for the study of neurological and psychiatric disorders. Progress report 1994--1997. Office of Scientific and Technical Information (OSTI), August 1999. http://dx.doi.org/10.2172/764610.

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Reiss, Michael. Type I Receptor Kinase Inhibitors - A Novel Treatment for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada408030.

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Fagan, Dedra. Type-I Insulin-Like Growth Factor Receptor (IGF1R)-Estrogen Receptor (ER) Crosstalk Contributes to Antiestrogen Therapy Resistance in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, February 2013. http://dx.doi.org/10.21236/ada575846.

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Reise, Michael. TGF-beta Type I Receptor Kinase Inhibitors - A Novel Treatment for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada416442.

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Rausch, Matthew. Enhancement of Dendritic Cell-Based Immunotherapy Using a Small Molecule TGF-beta Receptor Type I Kinase Inhibitor. Fort Belvoir, VA: Defense Technical Information Center, June 2008. http://dx.doi.org/10.21236/ada487435.

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Plymate, Stephen R. Therapy of Prostate Cancer Using a Human Antibody Targeting the Type 1 Insulin-Like Growth Factor Receptor (IGF-IR). Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada524529.

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Thomas, Tania, S. Shappell, S. Kasper, R. A. Serra, and H. L. Moses. The Development and Characterization of a Transgenic Mouse Model Over-Expressing a Truncated TGF(Beta) Type II Receptor in the Prostate. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada390670.

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Zhuo, Chuanjun, Hongjun Tian, Lina Wang, Xiangyang Gao, Li Ding, and Ming Liu. Comparative safety of glucagon like peptide‑1 receptor agonists in patients with type 2 diabetes: a network meta-analysis of cardiovascular outcome trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0122.

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Deo, Salil, David McAllister, Naveed Sattar, and Jill Pell. The time-varying cardiovascular benefits of glucagon like peptide-1 agonist (GLP-RA)therapy in patients with type 2 diabetes mellitus: A meta-analysis of multinational randomized trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0097.

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Abstract:
Review question / Objective: P - patients with type 2 diabetes melllitus already receiving routine medical therapy; I - patients receiving glucagon like peptide 1 receptor agonist (GLP1 receptor agonist) therapy (semaglutide, dulaglutide, liraglutide, exenatide, lixisenatide, efpeglenatide, abiglutide); C - patients receiving standard therapy for diabetes mellitus but not receiving GLP1 agonist therapy; O - composite end point as per invididual trial, cardiovascular mortality, all-cause mortality, myocardial infarction, stoke. Condition being studied: Type 2 diabetes mellitus. Study designs to be included: Randomised controlled trials which enroll a large number of patients (defined as > 500) and are multinational in origin. Studies included will need to have published Kaplan and Meier curves for the end-points presented in the manuscript.
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