Dopamine receptor - wikipedia Dopamine receptor Dopamine Dopamine receptors are a class of G protein - coupled receptors that are prominent in the vertebrate central nervous system ( CNS ). The neurotransmitter dopamine is the primary endogenous ligand for dopamine receptors. Dopamine receptors are implicated in many neurological processes, including motivation, pleasure, cognition, memory, learning, and fine motor control, as well as modulation of neuroendocrine signaling. Abnormal dopamine receptor signaling and dopaminergic nerve function is implicated in several neuropsychiatric disorders. Thus, dopamine receptors are common neurologic drug targets ; antipsychotics are often dopamine receptor antagonists while psychostimulants are typically indirect agonists of dopamine receptors. Contents 1 Subtypes 1.1 D - like family 1.2 D - like family 1.3 Receptor heteromers 2 Signalling mechanism 2.1 cAMP independent 3 Role in the central nervous system 4 Non-CNS dopamine receptors 4.1 Cardio - pulmonary system 4.2 Renal system 5 In disease 5.1 Attention - deficit hyperactivity disorder 5.2 Addictive drugs 5.3 Schizophrenia 5.4 Genetic hypertension 6 Dopamine regulation 7 See also 8 References 9 External links Subtypes This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. ( March 2009 ) The existence of multiple types of receptors for dopamine was first proposed in 1976. There are at least five subtypes of dopamine receptors, D, D, D, D, and D. The D and D receptors are members of the D - like family of dopamine receptors, whereas the D, D and D receptors are members of the D - like family. There is also some evidence that suggests the existence of possible D and D dopamine receptors, but such receptors have not been conclusively identified. At a global level, D receptors have widespread expression throughout the brain. Furthermore, D receptor subtypes are found at 10 - 100 times the levels of the D subtypes. D - like family The D - like family receptors are coupled to the G protein G. D is also coupled to G. G subsequently activates adenylyl cyclase, increasing the intracellular concentration of the second messenger cyclic adenosine monophosphate ( cAMP ). D is encoded by the Dopamine receptor D gene ( DRD1 ). D is encoded by the Dopamine receptor D gene ( DRD5 ). D - like family The D - like family receptors are coupled to the G protein G, which directly inhibits the formation of cAMP by inhibiting the enzyme adenylyl cyclase. D is encoded by the Dopamine receptor D gene ( DRD2 ), of which there are two forms : D Sh ( short ) and D Lh ( long ) : The D Sh form is pre-synaptically situated, having modulatory functions ( viz., autoreceptors, which regulate neurotransmission via feedback mechanisms. It affects synthesis, storage, and release of dopamine into the synaptic cleft ). The D Lh form may function as a classical post-synaptic receptor, i.e., transmit information ( in either an excitatory or an inhibitory fashion ) unless blocked by a receptor antagonist or a synthetic partial agonist. D is encoded by the Dopamine receptor D gene ( DRD3 ). Maximum expression of dopamine D receptors is noted in the islands of Calleja and nucleus accumbens. D is encoded by the Dopamine receptor D gene ( DRD4 ). The D receptor gene displays polymorphisms that differ in a variable number tandem repeat present within the coding sequence of exon 3. Some of these alleles are associated with greater incidence of certain disorders. For example, the D alleles have an established association with attention - deficit hyperactivity disorder. Receptor heteromers Dopamine receptors have been shown to heterodimerize with a number of other G protein - coupled receptors. The resulting dopamine receptor heterodimers include : D -- adenosine A D -- D dopamine receptor heteromer D -- D dopamine receptor heteromer D -- D dopamine receptor heteromer D -- adenosine A D -- ghrelin receptor D -- TAAR1 ( an autoreceptor heterodimer ) D -- adrenoceptor α D -- adrenoceptor β Signalling mechanism Dopamine receptor D and Dopamine receptor D are G coupled receptors that stimulate adenylyl cyclase to produce cAMP, increasing intracellular calcium among other cAMP mediated processes. The D2 class of receptors produce the opposite effect, as they are G coupled receptors, and block the activity of adenylyl cyclase. cAMP mediated protein kinase A activity also results in the phosphorylation of DARPP - 32, an inhibitor of protein phosphatase 1. Sustained D1 receptor activity is kept in check by Cyclin - dependent kinase 5. Dopamine receptor activation of Ca / calmodulin - dependent protein kinase II can be cAMP dependent or independent. The cAMP mediated pathway results in amplification of PKA phosphorylation activity, which is normally kept in equilibrium by PP1. The DARPP - 32 mediated PP1 inhibition amplifies PKA phosphorylation of AMPA, NMDA, and inward rectifying potassium channels, increasing AMPA and NMDA currents while decreasing potassium conductance. CAMP independent D1 receptor agonism and D2 receptor blockade also increases mRNA translation by phosphorylating ribosomal protein s6, resulting in activation of mTOR. The behavioral implications are unknown. Dopamine receptors may also regulate ion channels and BDNF independent of cAMP, possibly through direct interactions. There is evidence that D1 receptor agonism regulates phospholipase C independent of cAMP, however implications and mechanisms remain poorly understood. D2 receptor signaling may mediate protein kinase B, arrestin beta 2, and GSK - 3 activity, and inhibition of these proteins results in stunting of the hyperlocomotion in amphetamine treated rats. Dopamine receptors can also transactivate Receptor tyrosine kinases. Beta Arrestin recruitment is mediated by G - protein kinases that phosphorylate and inactivate dopamine receptors after stimulation. While beta arrestin plays a role in receptor desensitization, it may also be critical in mediating downstream effects of dopamine receptors. Beta arrestin has been shown to form complexes with MAP kinase, leading to activation of Extracellular signal -- regulated kinases. Furthermore, this pathway has been demonstrated to be involved in the locomotor response mediated by dopamine receptor D1. Dopamine receptor D2 stimulation results in the formation of an Atk / Beta - arrestin / PP2A protein complex that inhibits Atk through PP2A phosphorylation, therefore disinhibiting GSK - 3. Role in the central nervous system Further information : Neurotransmitter § Brain neurotransmitter systems Further information : Dopaminergic pathways Dopamine receptors control neural signaling that modulates many important behaviors, such as spatial working memory. Dopamine also plays an important role in the reward system, incentive salience, cognition, prolactin release, emesis and motor function. Non-cns dopamine receptors Cardio - pulmonary system In humans, the pulmonary artery expresses D, D, D, and D and receptor subtypes, which may account for vasodilatory effects of dopamine in the blood. In rats, D - like receptors are present on the smooth muscle of the blood vessels in most major organs. D receptors have been identified in the atria of rat and human hearts. Dopamine increases myocardial contractility and cardiac output, without changing heart rate, by signaling through dopamine receptors. Renal system Dopamine receptors are present along the nephron in the kidney, with proximal tubule epithelial cells showing the highest density. In rats, D - like receptors are present on the juxtaglomerular apparatus and on renal tubules, while D - like receptors are present on the glomeruli, zona glomerulosa cells of the adrenal cortex, renal tubules, and postganglionic sympathetic nerve terminals. Dopamine signaling affects diuresis and natriuresis. In disease Dysfunction of dopaminergic neurotransmission in the CNS has been implicated in a variety of neuropsychiatric disorders, including social phobia, Tourette 's syndrome, Parkinson 's disease, schizophrenia, neuroleptic malignant syndrome, attention - deficit hyperactivity disorder ( ADHD ), and drug and alcohol dependence. Attention - deficit hyperactivity disorder Dopamine receptors have been recognized as important components in the mechanism of ADHD for many years. Drugs used to treat ADHD, including methylphenidate and amphetamine, have significant effects on neuronal dopamine signaling. Studies of gene association have implicated several genes within dopamine signaling pathways ; in particular, the D variant of D has been consistently shown to be more frequent in ADHD patients. ADHD patients with the 4.7 allele also tend to have better cognitive performance and long - term outcomes compared to ADHD patients without the 4.7 allele, suggesting that the allele is associated with a more benign form of ADHD. The D allele has suppressed gene expression compared to other variants. Addictive drugs Main article : ΔFosB Dopamine is the primary neurotransmitter involved in the reward pathway in the brain. Thus, drugs that increase dopamine signaling may produce euphoric effects. Many recreational drugs, such as cocaine and substituted amphetamines, inhibit the dopamine transporter ( DAT ), the protein responsible for removing dopamine from the neural synapse. When DAT activity is blocked, the synapse floods with dopamine and increases dopaminergic signaling. When this occurs, particularly in the nucleus accumbens, increased D and decreased D receptor signaling mediates the `` rewarding '' stimulus of drug intake. Schizophrenia Main article : Dopamine hypothesis of schizophrenia While there is evidence that the dopamine system is involved in schizophrenia, the theory that hyperactive dopaminergic signal transduction induces the disease is controversial. Psychostimulants, such as amphetamine and cocaine, indirectly increase dopamine signaling ; large doses and prolonged use can induce symptoms that resemble schizophrenia. Additionally, many antipsychotic drugs target dopamine receptors, especially D receptors. Genetic hypertension Dopamine receptor mutations can cause genetic hypertension in humans. This can occur in animal models and humans with defective dopamine receptor activity, particularly D. Dopamine regulation See also : Yerkes -- Dodson law Dopamine receptors are typically stable, however sharp ( and sometimes prolonged ) increases or decreases in dopamine levels can downregulate ( reduce the numbers of ) or upregulate ( increase the numbers of ) dopamine receptors. Haloperidol, and some other antipsychotics, have been shown to increase the binding capacity of the D receptor when used over long periods of time ( i.e. increasing the number of such receptors ). Haloperidol increased the number of binding sites by 98 % above baseline in the worst cases, and yielded significant dyskinesia side effects. Addictive stimuli have variable effects on dopamine receptors, depending on the particular stimulus. According to one study, cocaine, heroin, amphetamine, alcohol, and nicotine cause decreases in D receptor quantity. A similar association has been linked to food addiction, with a low availability of dopamine receptors present in people with greater food intake. A recent news article summarized a U.S. DOE Brookhaven National Laboratory study showing that increasing dopamine receptors with genetic therapy temporarily decreased cocaine consumption by up to 75 %. The treatment was effective for 6 days. Cocaine upregulates D receptors in the nucleus accumbens, possibly contributing to drug seeking behavior. Certain stimulants will enhance cognition in the general population ( e.g., direct or indirect mesocortical DRD1 agonists as a class ), but only when used at low ( therapeutic ) concentrations. Relatively high doses of dopaminergic stimulants will result in cognitive deficits. Summary of addiction - related plasticity Form of neuroplasticity or behavioral plasticity Type of reinforcer Sources Opiates Psychostimulants High fat or sugar food Sexual intercourse Physical exercise ( aerobic ) Environmental enrichment ΔFosB expression in nucleus accumbens D1 - type MSNs ↑ ↑ ↑ ↑ ↑ ↑ Behavioral plasticity Escalation of intake Yes Yes Yes Psychostimulant cross-sensitization Yes Not applicable Yes Yes Attenuated Attenuated Psychostimulant self - administration ↑ ↑ ↓ ↓ ↓ Psychostimulant conditioned place preference ↑ ↑ ↓ ↑ ↓ ↑ Reinstatement of drug - seeking behavior ↑ ↑ ↓ ↓ Neurochemical plasticity CREB phosphorylation in the nucleus accumbens ↓ ↓ ↓ ↓ ↓ Sensitized dopamine response in the nucleus accumbens No Yes No Yes Altered striatal dopamine signaling ↓ DRD2, ↑ DRD3 ↑ DRD1, ↓ DRD2, ↑ DRD3 ↑ DRD1, ↓ DRD2, ↑ DRD3 ↑ DRD2 ↑ DRD2 Altered striatal opioid signaling No change or ↑ μ - opioid receptors ↑ μ - opioid receptors ↑ κ - opioid receptors ↑ μ - opioid receptors ↑ μ - opioid receptors No change No change Changes in striatal opioid peptides ↑ dynorphin No change : enkephalin ↑ dynorphin ↓ enkephalin ↑ dynorphin ↑ dynorphin Mesocorticolimbic synaptic plasticity Number of dendrites in the nucleus accumbens ↓ ↑ ↑ Dendritic spine density in the nucleus accumbens ↓ ↑ ↑ See also D2 short ( presynaptic ) Category : Dopamine agonists Category : Dopamine antagonists References Jump up ^ Girault JA, Greengard P ( 2004 ). `` The neurobiology of dopamine signaling ''. 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PMC 3139704. PMID 21459101. doi : 10.1016 / j. neuropharm. 2011.03. 010. Cross-sensitization is also bidirectional, as a history of amphetamine administration facilitates sexual behavior and enhances the associated increase in NAc DA... As described for food reward, sexual experience can also lead to activation of plasticity - related signaling cascades. The transcription factor delta FosB is increased in the NAc, PFC, dorsal striatum, and VTA following repeated sexual behavior ( Wallace et al., 2008 ; Pitchers et al., 2010b ). This natural increase in delta FosB or viral overexpression of delta FosB within the NAc modulates sexual performance, and NAc blockade of delta FosB attenuates this behavior ( Hedges et al, 2009 ; Pitchers et al., 2010b ). Further, viral overexpression of delta FosB enhances the conditioned place preference for an environment paired with sexual experience ( Hedges et al., 2009 )... In some people, there is a transition from `` normal '' to compulsive engagement in natural rewards ( such as food or sex ), a condition that some have termed behavioral or non-drug addictions ( Holden, 2001 ; Grant et al., 2006a )... In humans, the role of dopamine signaling in incentive - sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. This syndrome is characterized by a medication - induced increase in ( or compulsive ) engagement in non-drug rewards such as gambling, shopping, or sex ( Evans et al, 2006 ; Aiken, 2007 ; Lader, 2008 ). '' Table 1 '' Jump up ^ Fehr C, et al. ( 2008 ). `` Association of low striatal dopamine d2 receptor availability with nicotine dependence similar to that seen with other drugs of abuse ''. Am J Psychiatry. 165 ( 4 ) : 507 -- 14. PMID 18316420. doi : 10.1176 / appi. ajp. 2007.07020352. 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The present meta - analysis was conducted to estimate the magnitude of the effects of methylphenidate and amphetamine on cognitive functions central to academic and occupational functioning, including inhibitory control, working memory, short - term episodic memory, and delayed episodic memory. In addition, we examined the evidence for publication bias. Forty - eight studies ( total of 1,409 participants ) were included in the analyses. We found evidence for small but significant stimulant enhancement effects on inhibitory control and short - term episodic memory. Small effects on working memory reached significance, based on one of our two analytical approaches. Effects on delayed episodic memory were medium in size. However, because the effects on long - term and working memory were qualified by evidence for publication bias, we conclude that the effect of amphetamine and methylphenidate on the examined facets of healthy cognition is probably modest overall. In some situations, a small advantage may be valuable, although it is also possible that healthy users resort to stimulants to enhance their energy and motivation more than their cognition... Earlier research has failed to distinguish whether stimulants ' effects are small or whether they are nonexistent ( Ilieva et al., 2013 ; Smith & Farah, 2011 ). The present findings supported generally small effects of amphetamine and methylphenidate on executive function and memory. Specifically, in a set of experiments limited to high - quality designs, we found significant enhancement of several cognitive abilities... The results of this meta - analysis can not address the important issues of individual differences in stimulant effects or the role of motivational enhancement in helping perform academic or occupational tasks. However, they do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size. ^ Jump up to : Malenka RC, Nestler EJ, Hyman SE ( 2009 ). `` Chapter 13 : Higher Cognitive Function and Behavioral Control ''. In Sydor A, Brown RY. Molecular Neuropharmacology : A Foundation for Clinical Neuroscience ( 2nd ed. ). New York : McGraw - Hill Medical. p. 318. ISBN 9780071481274. Mild dopaminergic stimulation of the prefrontal cortex enhances working memory... Therapeutic ( relatively low ) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in normal subjects and those with ADHD. Positron emission tomography ( PET ) demonstrates that methylphenidate decreases regional cerebral blood flow in the doroslateral prefrontal cortex and posterior parietal cortex while improving performance of a spatial working memory task. This suggests that cortical networks that normally process spatial working memory become more efficient in response to the drug... ( It ) is now believed that dopamine and norepinephrine, but not serotonin, produce the beneficial effects of stimulants on working memory. At abused ( relatively high ) doses, stimulants can interfere with working memory and cognitive control... stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks... through indirect stimulation of dopamine and norepinephrine receptors. ^ Jump up to : Wood S, Sage JR, Shuman T, Anagnostaras SG ( January 2014 ). `` Psychostimulants and cognition : a continuum of behavioral and cognitive activation ''. Pharmacol. Rev. 66 ( 1 ) : 193 -- 221. PMID 24344115. doi : 10.1124 / pr. 112.007054. External links `` Dopamine Receptors ''. IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology. Zimmerberg, B., `` Dopamine receptors : A representative family of metabotropic receptors, Multimedia Neuroscience Education Project ( 2002 ) Scholarpedia article on Dopamine anatomy Cell surface receptor : G protein -- coupled receptors Class A : Rhodopsin - like Neurotransmitter Adrenergic α1 ( A D ) α2 ( A C ) β1 β2 β3 Purinergic Adenosine ( A1 A2A A2B A3 ) P2Y ( 1 5 6 8 9 10 11 12 13 14 ) Serotonin ( all but 5 - HT3 ) 5 - HT1 ( A F ) 5 - HT2 ( A C ) 5 - HT ( 4 5A 6 7 ) Other Acetylcholine ( M1 M2 M3 M4 M5 ) Dopamine D1 D2 D3 D4 D5 GHB receptor Histamine H1 H2 H3 H4 Melatonin ( 1A 1B 1C ) TAAR ( 1 5 6 8 9 ) Metabolites and signaling molecules Eicosanoid CysLT ( 1 2 ) LTB4 FPRL1 OXE Prostaglandin DP ( 1 2 ), EP ( 1 4 ), FP Prostacyclin Thromboxane Other Bile acid Cannabinoid ( CB1 CB2, GPR ( 18 55 119 ) ) EBI2 Estrogen Free fatty acid ( 1 4 ) Lactate Lysophosphatidic acid ( 1 5 6 ) Lysophospholipid ( 1 5 6 7 8 ) Niacin ( 1 2 ) Oxoglutarate PAF Sphingosine - 1 - phosphate ( 1 5 ) Succinate Peptide Neuropeptide B / W ( 1 2 ) FF ( 1 2 ) Y ( 1 5 ) Neuromedin ( B U ( 1 2 ) ) Neurotensin ( 1 2 ) Other Anaphylatoxin ( C3a C5a ) Angiotensin ( 1 2 ) Apelin Bombesin BRS3 GRPR NMBR ) Bradykinin ( B1 B2 ) Chemokine Cholecystokinin ( A B) Endothelin Formyl peptide ( 1 3 ) FSH Galanin ( 1 3 ) Gonadotropin - releasing hormone ( 1 2 ) Ghrelin Kisspeptin Luteinizing hormone / choriogonadotropin MAS ( 1 1L X1 X2 X3 X4 ) Melanocortin ( 1 5 ) MCHR ( 1 2 ) Motilin Opioid ( Delta Kappa Mu Nociceptin & Zeta, but not Sigma ) Orexin ( 1 2 ) Oxytocin Prokineticin ( 1 2 ) Prolactin - releasing peptide Relaxin ( 1 4 ) Somatostatin ( 1 5 ) Tachykinin ( 1 3 ) Thyrotropin Thyrotropin - releasing hormone Urotensin - II Vasopressin ( 1A 1B 2 ) Miscellaneous Orphan GPR ( 1 6 12 15 17 18 19 20 21 22 23 25 26 27 31 32 33 34 35 37 39 42 44 45 50 52 55 61 62 63 65 68 75 77 78 81 82 83 84 85 87 88 92 101 103 109A 109B 119 120 132 135 137B 139 141 142 146 148 149 150 151 152 153 160 161 162 171 173 174 176 177 182 183 ) Other Adrenomedullin Olfactory Opsin ( 3 5 1LW 1MW 1SW RGR RRH ) Protease - activated ( 1 4 ) SREB ( 1 3 ) Class B : Secretin - like Adhesion ADGRG ( 1 5 6 7 ) Orphan GPR ( 56 64 97 98 110 111 112 113 114 115 116 123 124 125 126 128 133 143 144 155 157 ) Other Brain - specific angiogenesis inhibitor ( 1 3 ) Cadherin ( 1 3 ) Calcitonin CALCRL CD97 Corticotropin - releasing hormone ( 1 2 ) EMR ( 1 3 ) Glucagon ( GR GIPR GLP1R GLP2R ) Growth - hormone - releasing hormone PACAPR1 GPR Latrophilin ( 1 ELTD1 ) Methuselah - like proteins Parathyroid hormone ( 1 2 ) Secretin Vasoactive intestinal peptide ( 1 2 ) Class C : Metabotropic glutamate / pheromone Taste TAS1R ( 1 3 ) TAS2R ( 1 5 7 8 9 10 13 14 16 19 20 30 31 38 39 40 41 42 43 45 46 50 60 Vomeronasal receptor ) Other Calcium - sensing receptor GABAB ( 1 2 ) Glutamate receptor ( Metabotropic glutamate ( 1 5 6 7 8 ) ) GPRC6A GPR ( 156 158 179 ) RAIG ( 1 4 ) Class F : Frizzled / Smoothened Frizzled Frizzled ( 1 5 6 7 8 9 10 ) Smoothened Smoothened Dopamine receptor modulators D - like Agonists Benzazepines : 6 - Br - APB Fenoldopam SKF - 38,393 SKF - 77,434 SKF - 81,297 SKF - 82,958 SKF - 83,959 Trepipam Zelandopam Ergolines : Cabergoline CY - 208,243 Dihydroergocryptine LEK - 8829 Lisuride Pergolide Terguride Dihydrexidine derivatives : A-77636 A-86929 Adrogolide ( ABT - 431, DAS - 431 ) Dihydrexidine Dinapsoline Dinoxyline Doxanthrine Phenethylamines : BCO - 001 Deoxyepinephrine ( N - methyldopamine, epinine ) Dopexamine Etilevodopa Ibopamine L - DOPA ( levodopa ) Melevodopa L - Phenylalanine L - Tyrosine XP21279 Others : A-68930 Apomorphine Isocorypalmine Nuciferine PF - 6649751 PF 6669571 Propylnorapomorphine Rotigotine SKF - 89,145 SKF - 89,626 Stepholidine Tetrahydropalmatine Antagonists Typical antipsychotics : Butaclamol Chlorpromazine Chlorprothixene Flupentixol ( flupenthixol ) ( + melitracen ) Fluphenazine Loxapine Perphenazine ( + amitriptyline ) Pifluthixol Thioridazine Thiothixene Trifluoperazine ( + tranylcypromine ) Zuclopenthixol Atypical antipsychotics : Asenapine Clorotepine Clotiapine Clozapine DHA - clozapine Fluperlapine Iloperidone Norclozapine Norquetiapine Olanzapine ( + + fluoxetine ) Paliperidone Quetiapine Risperidone Tefludazine Zicronapine Ziprasidone Zotepine Others : Berupipam Ecopipam EEDQ Metitepine ( methiothepin ) Odapipam Perlapine SCH - 23390 D - like Agonists Adamantanes : Amantadine Memantine Rimantadine Aminotetralins : 5 - OH - DPAT 7 - OH - DPAT 8 - OH - PBZI Rotigotine UH - 232 Ergolines : Bromocriptine Cabergoline Dihydroergocryptine Epicriptine Lisuride LSD Pergolide Terguride Dihydrexidine derivatives : 2 - OH - NPA Ciladopa Dihydrexidine Dinoxyline N, N - Propyldihydrexidine Phenethylamines : Deoxyepinephrine ( N - methyldopamine, epinine ) Dopexamine Etilevodopa Ibopamine L - DOPA ( levodopa ) L - Phenylalanine L - Tyrosine Melevodopa XP21279 Atypical antipsychotics : Alentemol ( U-66444B ) Aripiprazole ( + sertraline ) Aripiprazole lauroxil Bifeprunox Brexpiprazole Cariprazine F - 15063 Lumateperone Norclozapine RP5063 Others : 3 - PPP A-412,997 ABT - 670 ABT - 724 Adrafinil Aplindore Apomorphine Arketamine Armodafinil BP - 897 Captodiame CP - 226,269 Dizocilpine Esketamine Flibanserin GSK - 789,472 Ketamine Mesulergine Modafinil OSU - 6162 Pardoprunox PD - 128,907 PD - 168,077 PF - 219,061 PF - 592,379 Phencyclidine Piribedil Pramipexole Preclamol Propylnorapomorphine Pukateine Quinagolide Quinelorane Quinpirole RDS - 127 Ro10 - 5824 Ropinirole Roxindole Salvinorin A SKF - 83,959 Sumanirole Talipexole Umespirone WAY - 100,635 Antagonists Typical antipsychotics : Acepromazine Acetophenazine Azaperone Benperidol Bromperidol Butaclamol Butaperazine Chloracizine Chlorproethazine Chlorpromazine Chlorprothixene Ciclindole Clopenthixol Clothixamide Clopimozide Droperidol Fluacizine Fluanisone Flucindole Fluotracen Flupentixol ( flupenthixol ) ( + melitracen ) Fluphenazine Fluprothixene Fluspirilene Haloperidol Homopipramol Lenperone Levomepromazine ( methotrimeprazine ) Levosulpiride Loxapine Mesoridazine Moperone Naranol Nemonapride Penfluridol Perathiepin Perazine Pericyazine ( periciazine ) Perphenazine ( + amitriptyline ) Piflutixol ( pifluthixol ) Pimozide Pipamperone Preclamol Prochlorperazine Promazine Prothipendyl Spiperone ( spiroperidol ) Sulforidazine Sulpiride Sultopride Teflutixol Thiopropazate Thioproperazine Thioridazine Thiothixene Timiperone Trifluoperazine ( + tranylcypromine ) Triflupromazine Trifluperidol Zetidoline Zuclopenthixol Atypical antipsychotics : Amisulpride Asenapine BL - 1020 Blonanserin Carpipramine Cinuperone Clocapramine Clorotepine Clotiapine ( clothiapine ) Clozapine Cyamemazine DHA - clozapine Dixyrazine Elopiprazole Flumezapine Fluperlapine Gevotroline Iloperidone Lurasidone Mazapertine Melperone Molindone Mosapramine Ocaperidone Olanzapine ( + fluoxetine ) Paliperidone Perospirone Piperacetazine Pipotiazine Piquindone Quetiapine Remoxipride Risperidone Sertindole Tefludazine Tenilapine Tiospirone Veralipride Zicronapine Ziprasidone Zotepine Antiemetics / gastroprokinetics / sedatives : Aceprometazine AS - 8112 Alimemazine Alizapride Benzquinamide Bromopride Clebopride Domperidone Eticlopride Hydroxyzine Itopride Metoclopramide Metopimazine Promethazine Thiethylperazine Trimethobenzamide Antidepressants : Amoxapine Nefazodone Opipramol Propiomazine Trimipramine Others : 3 - PPP Azapride Buspirone Desmethoxyfallypride EEDQ F - 15063 Fallypride Fananserin Fenfluramine GSK - 789,472 Iodobenzamide Isocorypalmine L - 741,626 L - 745,870 Levofenfluramine LEK - 8829 Metergoline Metitepine ( methiothepin ) N - Methylspiperone Nafadotride Nuciferine PNU - 99,194 Pridopidine Raclopride Sarizotan SB - 277,011 - A Seridopidine Sonepiprazole Spiroxatrine Stepholidine SV - 293 Tetrahydropalmatine Tiapride UH - 232 Yohimbine See also : Receptor / signaling modulators Adrenergics Serotonergics Monoamine reuptake inhibitors Monoamine releasing agents Monoamine metabolism modulators Monoamine neurotoxins Retrieved from `` https://en.wikipedia.org/w/index.php?title=Dopamine_receptor&oldid=798092590 '' Categories : Dopamine receptors Hidden categories : Articles needing additional references from March 2009 All articles needing additional references All articles with unsourced statements Articles with unsourced statements from March 2009 Talk Contents About Wikipedia Deutsch Español Français Italiano 日本 語 Português Русский Српски / srpski Srpskohrvatski / српскохрватски Suomi Svenska ไทย Українська Edit links This page was last edited on 30 August 2017, at 23 : 15. 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Question: where are the dopamine receptors located in the brain
Answer: reward pathway