The Physiology, Signaling, and Pharmacology of Dopamine Receptors

Pharmacological Reviews, Год журнала: 2011, Номер 63(1), С. 182 - 217

Опубликована: Фев. 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.

Язык: Английский

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The glutamate homeostasis hypothesis of addiction

Nature reviews. Neuroscience, Год журнала: 2009, Номер 10(8), С. 561 - 572

Опубликована: Июль 1, 2009

Язык: Английский

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Toward a model of drug relapse: an assessment of the validity of the reinstatement procedure

Psychopharmacology, Год журнала: 2006, Номер 189(1), С. 1 - 16

Опубликована: Сен. 22, 2006

Язык: Английский

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Neurobiology of the incubation of drug craving

Trends in Neurosciences, Год журнала: 2011, Номер 34(8), С. 411 - 420

Опубликована: Июль 24, 2011

Язык: Английский

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Dopamine neurons encode the better option in rats deciding between differently delayed or sized rewards

Nature Neuroscience, Год журнала: 2007, Номер 10(12), С. 1615 - 1624

Опубликована: Ноя. 18, 2007

Язык: Английский

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Neuroplasticity in the mesolimbic dopamine system and cocaine addiction

British Journal of Pharmacology, Год журнала: 2008, Номер 154(2), С. 327 - 342

Опубликована: Март 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.

Язык: Английский

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A Memory Retrieval-Extinction Procedure to Prevent Drug Craving and Relapse

Science, Год журнала: 2012, Номер 336(6078), С. 241 - 245

Опубликована: Апрель 12, 2012

Drug use and relapse involve learned associations between drug-associated environmental cues drug effects. Extinction procedures in the clinic can suppress conditioned responses to cues, but extinguished typically reemerge after exposure itself (reinstatement), environment (renewal), or passage of time (spontaneous recovery). We describe a memory retrieval-extinction procedure that decreases effects seeking rat models relapse, craving abstinent heroin addicts. In rats, daily retrieval memories 10 minutes 1 hour not 6 hours before extinction sessions attenuated drug-induced reinstatement, spontaneous recovery, renewal seeking. addicts, cue-induced 1, 30, 180 days later. The is promising nonpharmacological method for decreasing during abstinence.

Язык: Английский

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Molecular Substrates for Retrieval and Reconsolidation of Cocaine-Associated Contextual Memory

Neuron, Год журнала: 2005, Номер 47(6), С. 873 - 884

Опубликована: Сен. 1, 2005

Язык: Английский

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MeCP2 controls BDNF expression and cocaine intake through homeostatic interactions with microRNA-212

Nature Neuroscience, Год журнала: 2010, Номер 13(9), С. 1120 - 1127

Опубликована: Авг. 15, 2010

Язык: Английский

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Addiction and Brain Reward and Antireward Pathways

Advances in psychosomatic medicine, Год журнала: 2011, Номер unknown, С. 22 - 60

Опубликована: Янв. 1, 2011

Addictive drugs have in common that they are voluntarily self-administered by laboratory animals (usually avidly), and enhance the functioning of reward circuitry brain (producing 'high' drug user seeks). The core consists an 'in-series' circuit linking ventral tegmental area, nucleus accumbens pallidum via medial forebrain bundle. Although originally believed to simply encode set point hedonic tone, these circuits now be functionally far more complex, also encoding attention, expectancy reward, disconfirmation expectancy, incentive motivation. 'Hedonic dysregulation' within may lead addiction. 'second-stage' dopaminergic component this is crucial addictive-drug-sensitive component. All addictive (directly or indirectly even transsynaptically) dop-aminergic synaptic function accumbens. Drug self-administration regulated dopamine levels, done keep a specific elevated range (to maintain desired level). For some classes (e.g. opiates), tolerance euphoric effects develops with chronic use. Postuse dysphoria then comes dominate addicts no longer use get high, but back normal ('get straight'). mediating pleasurable anatomically, neurophysiologically neurochemically different from those physical dependence, craving relapse. There important genetic variations vulnerability addiction, yet environmental factors such as stress social defeat alter brain-reward mechanisms manner impart In short, 'bio-psycho-social' model etiology holds very well for Addiction appears correlate hypodopaminergic dysfunctional state brain. Neuroimaging studies humans add credence hypothesis. Credible evidence implicates serotonergic, opioid, endocannabinoid, GABAergic glutamatergic Critically, addiction progresses occasional recreational impulsive habitual compulsive This correlates progression reward-driven habit-driven drug-seeking behavior. behavioral neuroanatomical striatal (nucleus accumbens) dorsal control over three classical sets relapse triggers (a) reexposure drugs, (b) stress, (c) cues (people, places, things) previously associated drug-taking Drug-triggered involves neurotransmitter dopamine. Stress-triggered central amygdala, bed stria terminalis, corticotrophin-releasing factor, lateral noradrenergic nuclei stem norepinephrine. Cue-triggered basolateral hippocampus glutamate. Knowledge neuroanatomy, neurophysiology, neurochemistry neuropharmacology action currently producing variety strategies pharmacotherapeutic treatment which appear promising.

Язык: Английский

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