The Physiology, Signaling, and Pharmacology of Dopamine Receptors

Pharmacological Reviews, Journal Year: 2011, Volume and Issue: 63(1), P. 182 - 217

Published: Feb. 8, 2011

G protein-coupled dopamine receptors (D1, D2, D3, D4, and D5) mediate all of the physiological functions catecholaminergic neurotransmitter dopamine, ranging from voluntary movement reward to hormonal regulation hypertension. Pharmacological agents targeting dopaminergic neurotransmission have been clinically used in management several neurological psychiatric disorders, including Parkinson9s disease, schizophrenia, bipolar disorder, Huntington9s attention deficit hyperactivity disorder (ADHD¹), Tourette9s syndrome. Numerous advances occurred understanding general structural, biochemical, functional properties that led development multiple pharmacologically active compounds directly target receptors, such as antiparkinson drugs antipsychotics. Recent progress complex biology receptor-related signal transduction mechanisms has revealed that, addition their primary action on cAMP-mediated signaling, can act through diverse signaling involve alternative protein coupling or protein-independent via interactions with ion channels proteins are characteristically implicated receptor desensitization, β-arrestins. One future directions managing dopamine-related pathologic conditions may a transition approaches affect function precise postreceptor intracellular modalities either ligand-biased pharmacology. In this comprehensive review, we discuss classification, basic structural genetic organization, distribution brain periphery, mechanisms. addition, abnormalities expression, function, documented human disorders current pharmacology emerging trends novel therapeutic at and/or related events.

Language: Английский

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Neurobiology of the incubation of drug craving

Trends in Neurosciences, Journal Year: 2011, Volume and Issue: 34(8), P. 411 - 420

Published: July 24, 2011

Language: Английский

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Opposing Patterns of Signaling Activation in Dopamine D₁and D₂Receptor-Expressing Striatal Neurons in Response to Cocaine and Haloperidol

Journal of Neuroscience, Journal Year: 2008, Volume and Issue: 28(22), P. 5671 - 5685

Published: May 28, 2008

Psychostimulants and other drugs of abuse activate extracellular signal-regulated kinase (ERK) in the striatum, through combined stimulation dopamine D 1 receptors (D1Rs) glutamate NMDA receptors. Antipsychotic similar signaling proteins striatum by blocking 2 (D2Rs). However, neurons which these pathways are activated psychotropic not precisely identified. We used transgenic mice, enhanced green fluorescent protein (EGFP) expression was driven D1R promoter ( drd1a -EGFP) or D2R drd2 -EGFP). confirmed -EGFP striatonigral striatopallidal neurons. Drd2 also expressed cholinergic interneurons, whereas no either detected GABAergic interneurons. Acute cocaine treatment increased phosphorylation ERK its direct indirect nuclear targets, mitogen- stress-activated kinase-1 (MSK1) histone H3, exclusively D1R-expressing output dorsal nucleus accumbens. Cocaine-induced c-Fos Zif268 predominated but observed D2R-expressing One week after repeated administration, cocaine-induced responses were decreased, with exception striatum. The remained confined to In contrast, acute haloperidol injection ERK, MSK1, H3 only induced c-fos zif268 predominantly Our results demonstrate that specifically two completely segregated populations striatal neurons, providing evidence for selective mechanisms exert their long-term effects.

Language: Английский

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Neuroplasticity in the mesolimbic dopamine system and cocaine addiction

British Journal of Pharmacology, Journal Year: 2008, Volume and Issue: 154(2), P. 327 - 342

Published: March 17, 2008

The main characteristics of cocaine addiction are compulsive drug use despite adverse consequences and high rates relapse during periods abstinence. A current popular hypothesis is that due to drug-induced neuroadaptations in reward-related learning memory processes, which cause hypersensitivity cocaine-associated cues, impulsive decision making abnormal habit-like learned behaviours insensitive consequences. Here, we review results from studies on the effect exposure selected signalling cascades, growth factors physiological processes previously implicated neuroplasticity underlying normal memory. These include extracellular signal-regulated kinase (ERK) pathway, brain-derived neurotrophic factor (BDNF), glutamate transmission, synaptic plasticity (primarily form long-term potentiation depression, LTP LTD). We also discuss degree these cocaine-induced changes mesolimbic dopamine system mediate psychomotor sensitization cocaine-seeking behaviours, as assessed animal models addiction. Finally, speculate how may interact initiate sustain seeking.

Language: Английский

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Epigenetic Mechanisms in Cognition

Neuron, Journal Year: 2011, Volume and Issue: 70(5), P. 813 - 829

Published: June 1, 2011

Language: Английский

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Opiate versus psychostimulant addiction: the differences do matter

Nature reviews. Neuroscience, Journal Year: 2011, Volume and Issue: 12(11), P. 685 - 700

Published: Oct. 5, 2011

Language: Английский

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Reversal of cocaine-evoked synaptic potentiation resets drug-induced adaptive behaviour

Nature, Journal Year: 2011, Volume and Issue: 481(7379), P. 71 - 75

Published: Dec. 6, 2011

Language: Английский

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Basal Ganglia Disorders Associated with Imbalances in the Striatal Striosome and Matrix Compartments

Frontiers in Neuroanatomy, Journal Year: 2011, Volume and Issue: 5

Published: Jan. 1, 2011

REVIEW article Front. Neuroanat., 07 September 2011 volume 5 - | https://doi.org/10.3389/fnana.2011.00059

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Natural rewards, neuroplasticity, and non-drug addictions

Neuropharmacology, Journal Year: 2011, Volume and Issue: 61(7), P. 1109 - 1122

Published: April 9, 2011

Language: Английский

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Cell Surface AMPA Receptors in the Rat Nucleus Accumbens Increase during Cocaine Withdrawal But Internalize after Cocaine Challenge in Association with Altered Activation of Mitogen-Activated Protein Kinases

Journal of Neuroscience, Journal Year: 2007, Volume and Issue: 27(39), P. 10621 - 10635

Published: Sept. 26, 2007

Although some studies report increased responsiveness of nucleus accumbens (NAc) AMPA receptors (AMPARs) after withdrawal from repeated cocaine treatment, others decreased plus challenge. Here we examine this apparent contradiction by quantifying cell surface and intracellular AMPAR subunits in the NAc before a challenge injection behaviorally sensitized rats. Because MAPKs (mitogen-activated protein kinases) regulate trafficking are implicated addiction, also evaluated phosphorylation extracellular signal-regulated kinase (ERK), c-Jun N-terminal (JNK), p38. Glutamate receptor 1 (GluR1) GluR2 surface/intracellular (S/I) ratios were 14 d rats but 24 h with (which elicited locomotor response) or saline conditioned locomotion). These findings suggested redistribution GluR1/2-containing receptors, possibility supported immunoprecipitation experiments indicating that most AMPARs GluR1/2 GluR2/3, few homomeric GluR1 GluR1/3 receptors. In rats, ERK during normalized JNK withdrawal, challenge, it was inversely related to S/I ratios. After p38 increased. summary, expression internalized single reexposure cocaine-related cues. paralleled expression. results complex, may be involved internalization respectively.

Language: Английский

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