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Bibliographies thématiques / Récepteur D1 de la dopamine / Livres

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Livres sur le sujet « Récepteur D1 de la dopamine »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 16 février 2022

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Consultez les 34 meilleurs livres pour votre recherche sur le sujet « Récepteur D1 de la dopamine ».

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1

Goldstein, Menek, Kjell Fuxe et Irving Tabachnick, dir. Central D1 Dopamine Receptors. Boston, MA : Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-2723-1.

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2

Breese, George R., et Ian Creese, dir. Neurobiology of Central D1-Dopamine Receptors. Boston, MA : Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5191-7.

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3

Blanchard, Jeffrey B. Functional implications of D1 and D2 dopamine receptors in dyskinesia. Sudbury, Ont : Laurentian University, Behavioural Neuroscience Program, 1997.

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4

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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5

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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6

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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7

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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8

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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9

Goldstein, M. J. Central D1 Dopamine Receptors. Springer, 2013.

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10

Central D1 dopamine receptors. Plenum, 1988.

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11

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

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12

R, Breese George, et Creese Ian, dir. Neurology of central D1-dopamine receptors. New York : Plenum, 1986.

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13

Neurobiology of Central D1-Dopamine Receptors. Springer, 1986.

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14

Breese, George. Neurobiology of Central D1-Dopamine Receptors. Springer, 2012.

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15

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

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16

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

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17

J, Vermeulen R., dir. The functional role of dopamine D1 receptors. Dordrecht : ICG Publications, 1994.

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18

Rajaram, Ryan D. Heterooligomerization of the D1 and D5 dopamine receptors. 2005.

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19

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

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20

Jarvie, Keith Roger. The glycoprotein nature of dopamine D1 and D2 receptors. 1990.

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21

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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22

Central D1 Dopamine Recep (Advances in Experimental Medicine and Biology). Plenum Press, 1988.

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23

Ng, Gordon Yiu Kon. Biochemial and pharmacological studies on dopamine D1 and D2L receptors. 1996.

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24

Bzowej, Natalie Helen. Dopamine D1 and D2 receptors in schizophrenia, Alzheimer's, Huntington's and Parkinson's diseases. 1990.

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25

Rapoza, Darion. The role of D1 and D2 dopamine receptors in the behavioral effects of cocaine. 1990.

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26

Beninger, Richard J. Mechanisms of dopamine-mediated incentive learning. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0012.

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Mechanisms of dopamine-mediated incentive learning explains how sensory events, resulting from an animal’s movement and the environment, activate cortical glutamatergic projections to dendritic spines of striatal medium spiny neurons to initiate a wave of phosphorylation. If no rewarding stimulus is encountered, a subsequent wave of phosphatase activity undoes the phosphorylation. If a rewarding stimulus is encountered, dopamine initiates a cascade of events in D1 receptor-expressing medium spiny neurons that may prevent the phosphatase effects and work synergistically with signaling events produced by glutamate. As a result, corticostriatal synapses have a greater impact on response systems; this may be part of the mechanism of incentive learning. Dopamine acting on dendritic spines of D2 receptor-expressing medium spiny neurons may prevent synaptic strengthening by inhibiting adenosine signaling; these synapses may be weakened through mechanisms involving endocannabinoids. When dopamine concentrations drop, e.g. during negative prediction errors, the opposite may occur, producing inverse incentive learning.

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27

Jin, Hui. Role of specific amino acid residues in the intracellular domains of human D1 dopamine receptors. 2000.

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28

Sunahara, Roger Ken. The molecular cloning and expression of the genes encoding the human dopamine D1 and D5 receptors. 1993.

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29

Functional interactions of D1 and D3 dopamine receptors : Generation and behavioural assessment of mice lacking both receptors. Ottawa : National Library of Canada, 2000.

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30

Karasinska, Joanna Monika. Spontaneous activity and cocaine-induced effects in mice lacking either dopamine D1 or D3, or both receptors. 2005.

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31

El-Ghundi, Mufida. Insights into the role of the dopamine D1 receptor in brain function : Studies using a gene deletion model. 2001.

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32

Kaar, Stephen J., Steven Potkin et Oliver Howes. The neurobiology of antipsychotic treatment response and resistance. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198828761.003.0005.

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Dopamine D2/3 receptor occupancy by antipsychotic drugs is central to clinical response and many of their side effects. Yet the locus of dopaminergic alterations in the majority of patients with schizophrenia is not the D2/3 receptor but, instead, presynaptic, comprising elevated striatal dopamine synthesis and release capacity. However, whilst this explains why dopamine D2/3 receptor blockade is effective in many patients, a proportion of patients does not respond. In some this is because of inadequate antipsychotic blockade of dopamine receptors, but there are others who do not respond to antipsychotic treatment despite substantial dopamine D2/3 receptor blockade. The neurobiology of treatment resistance does not seem to involve the presynaptic dopamine dysfunction typically seen in patients, suggesting that it needs different treatments. Disruptions to the glutamatergic system, and to dopamine D1 and D2/3 receptors and serotonin 2A receptors have all been proposed as potential mechanisms underlying treatment resistance and as targets for novel treatments.

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33

In vivo characterization of R/S-and R-[11C]SKF 82957 as a D1 agonist radioligand for pet : Effect of drugs acting on the dopamine system. Ottawa : National Library of Canada, 1998.

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34

Beninger, Richard J. Life's rewards. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.001.0001.

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Life’s Rewards: Linking Dopamine, Incentive Learning, Schizophrenia, and the Mind explains how increased brain dopamine produces reward-related incentive learning, the acquisition by neutral stimuli of increased ability to elicit approach and other responses. Dopamine decreases may produce inverse incentive learning, the loss by stimuli of the ability to elicit approach and other responses. Incentive learning is gradually lost when dopamine receptors are blocked. The brain has multiple memory systems defined as “declarative” and “non-declarative;” incentive learning produces one form of non-declarative memory. People with schizophrenia have hyperdopaminergia, possibly producing excessive incentive learning. Delusions may rely on declarative memory to interpret the world as it appears with excessive incentive learning. Parkinson’s disease, associated with dopamine loss, may involve a loss of incentive learning and increased inverse incentive learning. Drugs of abuse activate dopaminergic neurotransmission, leading to incentive learning about drug-associated stimuli. After withdrawal symptoms have been alleviated by detoxification treatment, drug-associated conditioned incentive stimuli will retain their ability to elicit responses until they are repeatedly experienced in the absence of primary drug rewards. Incentive learning may involve the action of dopamine at dendritic spines of striatal medium spiny neurons that have recently had glutamatergic input from assemblies of cortical neurons activated by environmental and proprioceptive stimuli. Glutamate initiates a wave of phosphorylation normally followed by a wave of phosphatase activity. If dopaminergic neurons fire, stimulation of D1 receptors prolongs the wave of phosphorylation, allowing glutamate synaptic strengthening. Activity in dopaminergic neurons in humans appears to affect mental experience.

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