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Książki na temat „Dopamine type I receptor”

Autor: Grafiati

Data publikacji: 19 października 2024

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1

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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2

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

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3

Tiberi, Mario, red. 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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4

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

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5

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

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6

Boileau, Isabelle, i Ginetta Collo, red. 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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7

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

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8

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

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9

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

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10

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

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11

O'Connor, Noreen A. D and D dopamine receptor signal transduction in transfected cell lines. Dublin: University College Dublin, 1998.

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12

Costanza, Rino Michelangelo. Dopamine receptor subtype involvement in the behavioural effects of cocaine. Birmingham: University of Birmingham, 1999.

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13

Lappalainen, Jaakko. Neurochemical and behavioural effects of dopamine D[sub]1 receptor blockade. Turku: J. Lappalainen, 1992.

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14

Malmberg, Åsa. Dopamine D2 and D3 receptor-ligand interactions: Molecular pharmacology and medicinal chemistry. Uppsala: Acta Universitatis Upsaliensis, 1996.

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15

Asghari, Vida. Structural, pharmacological, and functional characterization of polymorphic human dopamine D4 receptor isoforms. Ottawa: National Library of Canada, 1994.

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16

Sanyal, Suparna. Pharmacological and functional characterization of the polymorphic human dopamine D4 receptor isoforms. Ottawa: National Library of Canada, 1996.

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17

Hamadanizadeh, Soheila A. Pharmacological and functional differentiation of dopamine D1c and D1d receptor subtypes: Two novel members of the D1-like receptor family. Ottawa: National Library of Canada, 1996.

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18

elmhurst, Jennifer Lynne. characterization of the D3 dopamine receptor and a splice variant, D3NF, in SF9 cells. Ottawa: National Library of Canada, 1998.

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19

Tsatsos, Jim. Nicotine regulates opioid peptide and dopamine receptor gene expression in the rat brain and pituitary. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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20

Yano, Hideaki. Deconstructing G Protein-Coupled Receptor Dimer Pharmacology: Case Studies in Dopamine D1 and D2 Receptors. [New York, N.Y.?]: [publisher not identified], 2012.

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21

Rusk, Ilene Naomi. The effects of selective dopamine D [inferior] 1 and D [inferior] 2 agonists and antagonists on feeding and associated behaviour. Birmingham: University of Birmingham, 1989.

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22

Mukherjee, Tinku S. Regulation of the D1 dopamine receptor in rat brain and SK-N-Mc human neuroblastoma cells. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1995.

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23

Johnson, T. The preparation of some novel 2-[2-arylethyl]catecholamines required for evaluation as peripheral dopamine receptor agonists. Norwich: University of East Anglia, 1994.

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24

Lamey, Michael. Identification of distinct residues in the carboxyl tail regulating desensitization and internalization of the D1 dopamine receptor. Ottawa: National Library of Canada, 2000.

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25

Timothy V. P. C. Beischlag. Molecular cloning and characterization of the 5'-flanking and promoter region of the human dopamine D5 receptor gene. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1996.

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26

Sanci, Vito. Effect of chronic haloperidol, endogenous dopamine, and selective D1 competitors on in vivo D1 receptor binding in rat brain. Ottawa: National Library of Canada, 2000.

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27

Ko, Francoise Dulcinea. Effect of GABARAP (GABA(A)-receptor-associated protein on the interaction between the dopamine D(5) and GABA(A) receptors. Ottawa: National Library of Canada, 2001.

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28

Wigmore, Mark Aubrey. Depression of glutamate input and excitation of midbrain dopamine neurones by metabotropic glutamate receptor activation: An electrophysiological study in rat brain slices. Birmingham: University of Birmingham, 1997.

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29

Playford, Martin P. The role of the type 1 insulin-like growth factor receptor in cancer biology. Oxford: Oxford Brookes University, 2000.

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30

Johansson, P. J. Hugo. Herpes simplex virus type 1 induced IgG Fc receptor: Aspects of specificity and function. Lund: Univ., 1989.

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31

Cheung, Hermia. Effect of dopamine depletion on D1 receptor binding in rat brain; and metabolism studies of D1 agonist R-[11C]SKF 82957 and phosphodiesterase-4 inhibitor R-[11C}rolipram. Ottawa: National Library of Canada, 2003.

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32

1929-, Shigeta Yukio, Kobayashi Masashi Dr i Olefsky Jerrold M, red. Recent advances in insulin action and its disorders: Proceedings of the International Symposium on Insulin Action and Its Disorders, Shiga, 16 May 1990. Amsterdam: Excerpta Medica, 1991.

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33

Flavin, Nora. Cloning and characterisation of the bovine activin receptor type II gene (ActRII): Its localisation to chromosome 2 (BTA2) by somatic cell genetic analysis and the genotyping of an associated microsatelltie UCD2. Dublin: University College Dublin, 1996.

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34

(Editor), Peter Jenner, i R. Demirdamar (Editor), red. Dopamine Receptor Sub-Types: From Basic Sciences to Clinical Applications (Biomedical and Health Research, Vol. 19) (Biomedical and Health Research, V. 19). Ios Pr Inc, 1997.

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35

Nielsen, David A., Dmitri Proudnikov i Mary Jeanne Kreek. The Genetics of Impulsivity. Redaktorzy Jon E. Grant i Marc N. Potenza. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195389715.013.0080.

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Impulsivity is a complex trait that varies across healthy individuals, although when excessive, it is generally regarded as dysfunctional. Impulsive behavior may lead to initiation of drug addiction that interferes with inhibitory controls, which may in turn result in facilitation of the individual’s impulsive acts. Although environmental factors play a considerable role in impulsive behavior, a body of evidence collected in twin studies suggests that about 45% of the variance in impulsivity is accounted for by genetic factors. Genetic variants studied in association with impulsivity include those fortryptophan hydroxylase 1 and 2 (TPH1 and TPH2), the serotonintransporter (SERT), serotonin receptors, and genes of the monoamine metabolism pathway (e.g., monoamine oxidase A, MAOA). Other systems may also play a role in these behaviors, such as the dopaminergic system (the dopamine receptors DRD2, DRD3, and DRD4, and the dopamine transporter, DAT), the catecholaminergic system (catechol-O-methyltransferase, COMT), and the GABAergic system (GABAreceptor subunit alpha-1, GABRA1; GABA receptor subunit alpha-6, GABRA6; and GABA receptor subunit beta-1, GABRB1). Taking into account involvement of the hypothalamic-pituitary-adrenal (HPA) axis, the number of candidate genes implicated in impulsivity may be increased significantly and, therefore, may go far beyond those of serotonergic and dopaminergic systems. For a number of years, our group has conducted studies of the association of genes involved in the modulation of the stress-responsive HPA axis and several neurotransmitter systems, all involved in the pathophysiology of anxiety and depressive disorders, impulse control and compulsive disorders, with drug addiction. These genes include those of the opioid system: the mu- and kappa-opioid receptors (OPRM1 and OPRK1) and the nociceptin/orphaninFQ receptor (OPRL1); the serotonergic system: TPH1 and TPH2 and the serotonin receptor 1B (5THR1B); the catecholamine system: COMT; the HPA axis: themelanocortin receptor type 2 (MC2R or adrenocorticotropic hormone, ACTHR); and the cannabinoid system: the cannabinoid receptor type 1 (CNR1). In this chapter we will focus on these findings.

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36

Poste, George, i Stanley T. Crooke. Dopamine Receptor Agonists. Springer, 2013.

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37

Poste, George, i Stanley T. Crooke. Dopamine Receptor Agonists. Springer, 2012.

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38

Tiberi, Mario. Dopamine Receptor Technologies. Humana Press, 2016.

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39

Poste, George, i Stanley T. Crooke. Dopamine Receptor Agonists. Springer, 2013.

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40

Fox, Susan H. Delayed and Often Persistent. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0021.

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Tardive syndromes are drug-induced hyperkinetic movement disorders that occur as a consequence of dopamine D2 receptor antagonism/blockade. There are several types, including classical tardive dyskinesia, tardive dystonia, tardive tics, tardive myoclonus, and tardive tremor, and it is important to the management of these disorders that the type of movement disorder induced is identified. Tardive syndromes can occur with all antipsychotic drugs, including so-called atypical drugs. Patients taking these drugs should be evaluated frequently for side effects. Evaluating the nature of the movement (i.e., chorea or dystonia) is important because treatment options can differ according to the type of dyskinesia present.

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41

Otsuka, Norman Yoshinobu. Dopamine D r receptor solubilization. 1985.

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42

Sugamori, Kim S. The dopamine D1C receptor expansion and origin of the dopamine D1 receptor family. 1999.

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43

Beninger, Richard J. Dopamine receptor subtypes and incentive learning. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0007.

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Dopamine receptor subtypes and incentive learning explains that dopamine receptors are G protein-coupled and form two families: D1-like receptors, including D1 and D5, stimulate adenylyl cyclase and cyclic adenosine monophosphate (cAMP); D2-like receptors, including D2, D3, and D4, inhibit cAMP. Antipsychotic medications are dopamine receptor antagonists and their clinical potency is strongly correlated with blockade of D2 receptors, implicating overactivity of D2 receptors in psychosis in schizophrenia. D1- and D2-like receptors appear to be involved in unconditioned locomotor activity and incentive learning. D1-like receptors are implicated more strongly in incentive learning and D2-like receptors more strongly in locomotion. D3 receptors may play a relatively greater role in expression than acquisition of incentive learning. Dopamine receptor subtypes form heteromers with each other and with the receptors of other neurotransmitters (e.g., glutamate, adenosine, ghrelin) and the signaling properties of these heteromers can differ from those of either receptor in isolation.

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44

Lee, Samuel Paikwon. Oligomerization of the D2 dopamine receptor. 2004.

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45

Waddington, John L. D1: D2 Dopamine Receptor Interactions (Neuroscience Perspectives). Academic Press, 1993.

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46

Waddington, John L. D1: D2 Dopamine Receptor Interactions (Neuroscience Perspectives). Academic Press, 1993.

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47

Creese, Ian, i Claire M. Fraser. Dopamine Receptors (Receptor Biochemistry and Methodology, Vol 8). John Wiley & Sons, 1987.

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48

Oldenhof, John. SH3 binding domains in the dopamine D4 receptor. 1999.

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49

Borgundvaag, Bjug. Dopamine receptor mediated inhibition of anterior pituitary adenylate cyclose. 1985.

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50

Clozapine congeners: Structural requirements for dopamine D4 receptor selectivity. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1995.

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