Evidence against dopamine D1/D2 receptor heteromers

Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation, because their purported potential to manifest signaling and pharmacological properties that differ from the component receptors makes them highly attractive for the development of more selective pharmac...

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Published inMolecular psychiatry Vol. 20; no. 11; pp. 1373 - 1385
Main Authors Frederick, A L, Yano, H, Trifilieff, P, Vishwasrao, H D, Biezonski, D, Mészáros, J, Urizar, E, Sibley, D R, Kellendonk, C, Sonntag, K C, Graham, D L, Colbran, R J, Stanwood, G D, Javitch, J A
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.11.2015
Nature Publishing Group
Subjects
13/51
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine - analogs & derivatives
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine - pharmacology
42/44
631/378
64/60
9/10
96/33
Animals
Behavioral Sciences
Biological Psychology
Bioluminescence
Biosensors
Brain slice preparation
Corpus Striatum - drug effects
Corpus Striatum - metabolism
Depression, Mental
Dopamine
Dopamine Agonists - pharmacology
Dopamine Antagonists - pharmacology
Dopamine D1 receptors
Dopamine D2 receptors
Dopamine receptors
Drug therapy
G protein-coupled receptors
Grooming
Grooming - drug effects
GTP-Binding Protein alpha Subunits, Gq-G11 - genetics
GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism
HEK293 Cells
Humans
Kinases
Life Sciences
Ligands
Localization
Luminescent Proteins - genetics
Luminescent Proteins - metabolism
Male
Medicine
Medicine & Public Health
Mental disorders
Mice
Mice, Inbred C57BL
Mice, Knockout
Models, Molecular
Motor Activity - drug effects
Motor Activity - genetics
Mutants
Neurosciences
Nucleus accumbens
Nucleus Accumbens - drug effects
Nucleus Accumbens - metabolism
Oligomers
original-article
Pharmacology
Pharmacotherapy
Phospholipase C
Phosphorylation - drug effects
Physiological aspects
Protein Multimerization - drug effects
Protein Multimerization - physiology
Protein Structure, Tertiary
Proteins
Psychiatry
Receptor mechanisms
Receptors, Dopamine D1 - genetics
Receptors, Dopamine D1 - metabolism
Receptors, Dopamine D2 - genetics
Receptors, Dopamine D2 - metabolism
Risk factors
Schizophrenia
Signal transduction
United States
New York
United States > US
Nashville Tennessee
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Abstract Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation, because their purported potential to manifest signaling and pharmacological properties that differ from the component receptors makes them highly attractive for the development of more selective pharmacological treatments. In particular, dopamine D1 and D2 receptors have been proposed to form hetero-oligomers that couple to G αq proteins, and SKF83959 has been proposed to act as a biased agonist that selectively engages these receptor complexes to activate G αq and thus phospholipase C. D1/D2 heteromers have been proposed as relevant to the pathophysiology and treatment of depression and schizophrenia. We used in vitro bioluminescence resonance energy transfer, ex vivo analyses of receptor localization and proximity in brain slices, and behavioral assays in mice to characterize signaling from these putative dimers/oligomers. We were unable to detect G αq or G α11 protein coupling to homomers or heteromers of D1 or D2 receptors using a variety of biosensors. SKF83959-induced locomotor and grooming behaviors were eliminated in D1 receptor knockout (KO) mice, verifying a key role for D1-like receptor activation. In contrast, SKF83959-induced motor responses were intact in D2 receptor and G αq KO mice, as well as in knock-in mice expressing a mutant Ala 286 -CaMKIIα that cannot autophosphorylate to become active. Moreover, we found that, in the shell of the nucleus accumbens, even in neurons in which D1 and D2 receptor promoters are both active, the receptor proteins are segregated and do not form complexes. These data are not compatible with SKF83959 signaling through G αq or through a D1/D2 heteromer and challenge the existence of such a signaling complex in the adult animals that we used for our studies.
AbstractList Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation, because their purported potential to manifest signaling and pharmacological properties that differ from the component receptors makes them highly attractive for the development of more selective pharmacological treatments. In particular, dopamine D1 and D2 receptors have been proposed to form hetero-oligomers that couple to Gαq proteins, and SKF83959 has been proposed to act as a biased agonist that selectively engages these receptor complexes to activate Gαq and thus phospholipase C. D1/D2 heteromers have been proposed as relevant to the pathophysiology and treatment of depression and schizophrenia. We used in vitro bioluminescence resonance energy transfer, ex vivo analyses of receptor localization and proximity in brain slices, and behavioral assays in mice to characterize signaling from these putative dimers/oligomers. We were unable to detect Gαq or Gα11 protein coupling to homomers or heteromers of D1 or D2 receptors using a variety of biosensors. SKF83959-induced locomotor and grooming behaviors were eliminated in D1 receptor knockout (KO) mice, verifying a key role for D1-like receptor activation. In contrast, SKF83959-induced motor responses were intact in D2 receptor and Gαq KO mice, as well as in knock-in mice expressing a mutant Ala(286)-CaMKIIα that cannot autophosphorylate to become active. Moreover, we found that, in the shell of the nucleus accumbens, even in neurons in which D1 and D2 receptor promoters are both active, the receptor proteins are segregated and do not form complexes. These data are not compatible with SKF83959 signaling through Gαq or through a D1/D2 heteromer and challenge the existence of such a signaling complex in the adult animals that we used for our studies.Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation, because their purported potential to manifest signaling and pharmacological properties that differ from the component receptors makes them highly attractive for the development of more selective pharmacological treatments. In particular, dopamine D1 and D2 receptors have been proposed to form hetero-oligomers that couple to Gαq proteins, and SKF83959 has been proposed to act as a biased agonist that selectively engages these receptor complexes to activate Gαq and thus phospholipase C. D1/D2 heteromers have been proposed as relevant to the pathophysiology and treatment of depression and schizophrenia. We used in vitro bioluminescence resonance energy transfer, ex vivo analyses of receptor localization and proximity in brain slices, and behavioral assays in mice to characterize signaling from these putative dimers/oligomers. We were unable to detect Gαq or Gα11 protein coupling to homomers or heteromers of D1 or D2 receptors using a variety of biosensors. SKF83959-induced locomotor and grooming behaviors were eliminated in D1 receptor knockout (KO) mice, verifying a key role for D1-like receptor activation. In contrast, SKF83959-induced motor responses were intact in D2 receptor and Gαq KO mice, as well as in knock-in mice expressing a mutant Ala(286)-CaMKIIα that cannot autophosphorylate to become active. Moreover, we found that, in the shell of the nucleus accumbens, even in neurons in which D1 and D2 receptor promoters are both active, the receptor proteins are segregated and do not form complexes. These data are not compatible with SKF83959 signaling through Gαq or through a D1/D2 heteromer and challenge the existence of such a signaling complex in the adult animals that we used for our studies.
Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation, because their purported potential to manifest signaling and pharmacological properties that differ from the component receptors makes them highly attractive for the development of more selective pharmacological treatments. In particular, dopamine D1 and D2 receptors have been proposed to form hetero-oligomers that couple to Gαq proteins, and SKF83959 has been proposed to act as a biased agonist that selectively engages these receptor complexes to activate Gαq and thus phospholipase C. D1/D2 heteromers have been proposed as relevant to the pathophysiology and treatment of depression and schizophrenia. We used in vitro bioluminescence resonance energy transfer, ex vivo analyses of receptor localization and proximity in brain slices, and behavioral assays in mice to characterize signaling from these putative dimers/oligomers. We were unable to detect Gαq or Gα11 protein coupling to homomers or heteromers of D1 or D2 receptors using a variety of biosensors. SKF83959-induced locomotor and grooming behaviors were eliminated in D1 receptor knockout (KO) mice, verifying a key role for D1-like receptor activation. In contrast, SKF83959-induced motor responses were intact in D2 receptor and Gαq KO mice, as well as in knock-in mice expressing a mutant Ala286 -CaMKIIα that cannot autophosphorylate to become active. Moreover, we found that, in the shell of the nucleus accumbens, even in neurons in which D1 and D2 receptor promoters are both active, the receptor proteins are segregated and do not form complexes. These data are not compatible with SKF83959 signaling through Gαq or through a D1/D2 heteromer and challenge the existence of such a signaling complex in the adult animals that we used for our studies.
Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation, because their purported potential to manifest signaling and pharmacological properties that differ from the component receptors makes them highly attractive for the development of more selective pharmacological treatments. In particular, dopamine D1 and D2 receptors have been proposed to form hetero-oligomers that couple to Gαq proteins, and SKF83959 has been proposed to act as a biased agonist that selectively engages these receptor complexes to activate Gαq and thus phospholipase C. D1/D2 heteromers have been proposed as relevant to the pathophysiology and treatment of depression and schizophrenia. We used in vitro bioluminescence resonance energy transfer, ex vivo analyses of receptor localization and proximity in brain slices, and behavioral assays in mice to characterize signaling from these putative dimers/oligomers. We were unable to detect Gαq or Gα11 protein coupling to homomers or heteromers of D1 or D2 receptors using a variety of biosensors. SKF83959-induced locomotor and grooming behaviors were eliminated in D1 receptor knockout (KO) mice, verifying a key role for D1-like receptor activation. In contrast, SKF83959-induced motor responses were intact in D2 receptor and Gαq KO mice, as well as in knock-in mice expressing a mutant Ala(286)-CaMKIIα that cannot autophosphorylate to become active. Moreover, we found that, in the shell of the nucleus accumbens, even in neurons in which D1 and D2 receptor promoters are both active, the receptor proteins are segregated and do not form complexes. These data are not compatible with SKF83959 signaling through Gαq or through a D1/D2 heteromer and challenge the existence of such a signaling complex in the adult animals that we used for our studies.
Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation, because their purported potential to manifest signaling and pharmacological properties that differ from the component receptors makes them highly attractive for the development of more selective pharmacological treatments. In particular, dopamine D1 and D2 receptors have been proposed to form hetero-oligomers that couple to [G.sub.αq] proteins, and SKF83959 has been proposed to act as a biased agonist that selectively engages these receptor complexes to activate [G.sub.αq] and thus phospholipase C. D1/D2 heteromers have been proposed as relevant to the pathophysiology and treatment of depression and schizophrenia. We used in vitro bioluminescence resonance energy transfer, ex vivo analyses of receptor localization and proximity in brain slices, and behavioral assays in mice to characterize signaling from these putative dimers/oligomers. We were unable to detect [G.sub.αq] or [G.sub.α11] protein coupling to homomers or heteromers of D1 or D2 receptors using a variety of biosensors. SKF83959-induced locomotor and grooming behaviors were eliminated in D1 receptor knockout (KO) mice, verifying a key role for D1-like receptor activation. In contrast, SKF83959-induced motor responses were intact in D2 receptor and [G.sub.αq] KO mice, as well as in knock-in mice expressing a mutant [Ala.sup.286]-CaMKIIα that cannot autophosphorylate to become active. Moreover, we found that, in the shell of the nucleus accumbens, even in neurons in which D1 and D2 receptor promoters are both active, the receptor proteins are segregated and do not form complexes. These data are not compatible with SKF83959 signaling through [G.sub.αq] or through a D1/D2 heteromer and challenge the existence of such a signaling complex in the adult animals that we used for our studies. Molecular Psychiatry (2015) 20, 1373-1385; doi: 10.1038/mp.2014.166; published online 6 January 2015
Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation, because their purported potential to manifest signaling and pharmacological properties that differ from the component receptors makes them highly attractive for the development of more selective pharmacological treatments. In particular, dopamine D1 and D2 receptors have been proposed to form hetero-oligomers that couple to G αq proteins, and SKF83959 has been proposed to act as a biased agonist that selectively engages these receptor complexes to activate G αq and thus phospholipase C. D1/D2 heteromers have been proposed as relevant to the pathophysiology and treatment of depression and schizophrenia. We used in vitro bioluminescence resonance energy transfer, ex vivo analyses of receptor localization and proximity in brain slices, and behavioral assays in mice to characterize signaling from these putative dimers/oligomers. We were unable to detect G αq or G α11 protein coupling to homomers or heteromers of D1 or D2 receptors using a variety of biosensors. SKF83959-induced locomotor and grooming behaviors were eliminated in D1 receptor knockout (KO) mice, verifying a key role for D1-like receptor activation. In contrast, SKF83959-induced motor responses were intact in D2 receptor and G αq KO mice, as well as in knock-in mice expressing a mutant Ala 286 -CaMKIIα that cannot autophosphorylate to become active. Moreover, we found that, in the shell of the nucleus accumbens, even in neurons in which D1 and D2 receptor promoters are both active, the receptor proteins are segregated and do not form complexes. These data are not compatible with SKF83959 signaling through G αq or through a D1/D2 heteromer and challenge the existence of such a signaling complex in the adult animals that we used for our studies.
Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation, because their purported potential to manifest signaling and pharmacological properties that differ from the component receptors makes them highly attractive for the development of more selective pharmacological treatments. In particular, dopamine D1 and D2 receptors have been proposed to form hetero-oligomers that couple to [G.sub.αq] proteins, and SKF83959 has been proposed to act as a biased agonist that selectively engages these receptor complexes to activate [G.sub.αq] and thus phospholipase C. D1/D2 heteromers have been proposed as relevant to the pathophysiology and treatment of depression and schizophrenia. We used in vitro bioluminescence resonance energy transfer, ex vivo analyses of receptor localization and proximity in brain slices, and behavioral assays in mice to characterize signaling from these putative dimers/oligomers. We were unable to detect [G.sub.αq] or [G.sub.α11] protein coupling to homomers or heteromers of D1 or D2 receptors using a variety of biosensors. SKF83959-induced locomotor and grooming behaviors were eliminated in D1 receptor knockout (KO) mice, verifying a key role for D1-like receptor activation. In contrast, SKF83959-induced motor responses were intact in D2 receptor and [G.sub.αq] KO mice, as well as in knock-in mice expressing a mutant [Ala.sup.286]-CaMKIIα that cannot autophosphorylate to become active. Moreover, we found that, in the shell of the nucleus accumbens, even in neurons in which D1 and D2 receptor promoters are both active, the receptor proteins are segregated and do not form complexes. These data are not compatible with SKF83959 signaling through [G.sub.αq] or through a D1/D2 heteromer and challenge the existence of such a signaling complex in the adult animals that we used for our studies.
Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation because their purported potential to manifest signaling and pharmacological properties that differ from the component receptors makes them highly attractive for the development of more selective pharmacological treatments. In particular, dopamine D1 and D2 receptors have been proposed to form hetero-oligomers that couple to G αq proteins, and SKF83959 has been proposed to act as a biased agonist that selectively engages these receptor complexes to activate G αq and thus phospholipase C. D1/D2 heteromers have been proposed as relevant to the pathophysiology and treatment of depression and schizophrenia. We used in vitro bioluminescence resonance energy transfer (BRET), ex vivo analyses of receptor localization and proximity in brain slices, and behavioral assays in mice to characterize signaling from these putative dimers/oligomers. We were unable to detect G αq or G α11 protein coupling to homomers or heteromers of D1 or D2 receptors using a variety of biosensors. SKF83959-induced locomotor and grooming behaviors were eliminated in D 1 receptor knockout mice, verifying a key role for D1-like receptor activation. In contrast, SKF83959-induced motor responses were intact in D2 receptor and G αq knockout mice, as well as in knock-in mice expressing a mutant Ala 286 -CaMKIIα, that cannot autophosphorylate to become active. Moreover, we found that in the shell of the nucleus accumbens, even in neurons in which D1 and D2 receptor promoters are both active, the receptor proteins are segregated and do not form complexes. These data are not compatible with SKF83959 signaling through G αq or through a D1–D2 heteromer and challenge the existence of such a signaling complex in the adult animals that we used for our studies.
Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation, because their purported potential to manifest signaling and pharmacological properties that differ from the component receptors makes them highly attractive for the development of more selective pharmacological treatments. In particular, dopamine D1 and D2 receptors have been proposed to form hetero-oligomers that couple to G sub( alpha q) proteins, and SKF83959 has been proposed to act as a biased agonist that selectively engages these receptor complexes to activate G sub( alpha q) and thus phospholipase C. D1/D2 heteromers have been proposed as relevant to the pathophysiology and treatment of depression and schizophrenia. We used in vitro bioluminescence resonance energy transfer, ex vivo analyses of receptor localization and proximity in brain slices, and behavioral assays in mice to characterize signaling from these putative dimers/oligomers. We were unable to detect G sub( alpha q) or G sub( alpha 11) protein coupling to homomers or heteromers of D1 or D2 receptors using a variety of biosensors. SKF83959-induced locomotor and grooming behaviors were eliminated in D1 receptor knockout (KO) mice, verifying a key role for D1-like receptor activation. In contrast, SKF83959-induced motor responses were intact in D2 receptor and G sub( alpha q) KO mice, as well as in knock-in mice expressing a mutant Ala super(286)-CaMKII alpha that cannot autophosphorylate to become active. Moreover, we found that, in the shell of the nucleus accumbens, even in neurons in which D1 and D2 receptor promoters are both active, the receptor proteins are segregated and do not form complexes. These data are not compatible with SKF83959 signaling through G sub( alpha q) or through a D1/D2 heteromer and challenge the existence of such a signaling complex in the adult animals that we used for our studies.
Audience Academic
Author Sonntag, K C
Colbran, R J
Vishwasrao, H D
Stanwood, G D
Biezonski, D
Trifilieff, P
Sibley, D R
Kellendonk, C
Frederick, A L
Urizar, E
Yano, H
Javitch, J A
Mészáros, J
Graham, D L
AuthorAffiliation 1 Neuroscience Graduate Program, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
7 Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
8 Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
5 Molecular Neuropharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA
2 Departments of Psychiatry and Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York, USA
4 Center for Neuroscience. Columbia University, Kolb Research Building, New York, NY10032, USA
9 Vanderbilt Kennedy Center and Vanderbilt Brain Institute, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
6 Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA
3 Nutrition and Integrative Neurobiology, INRA UMR 1286; University of Bordeaux, F-33076, Bordeaux, France
10 Di
AuthorAffiliation_xml – name: 6 Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA
– name: 1 Neuroscience Graduate Program, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
– name: 7 Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
– name: 2 Departments of Psychiatry and Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York, USA
– name: 9 Vanderbilt Kennedy Center and Vanderbilt Brain Institute, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
– name: 3 Nutrition and Integrative Neurobiology, INRA UMR 1286; University of Bordeaux, F-33076, Bordeaux, France
– name: 10 Division of Molecular Therapeutics, New York State Psychiatric Institute, New York, New York, USA
– name: 4 Center for Neuroscience. Columbia University, Kolb Research Building, New York, NY10032, USA
– name: 5 Molecular Neuropharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA
– name: 8 Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
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  givenname: A L
  surname: Frederick
  fullname: Frederick, A L
  organization: Neuroscience Graduate Program, Vanderbilt University School of Medicine
– sequence: 2
  givenname: H
  surname: Yano
  fullname: Yano, H
  organization: Departments of Psychiatry and Pharmacology, College of Physicians and Surgeons, Columbia University, 12Current address: National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD 21224, USA
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  surname: Trifilieff
  fullname: Trifilieff, P
  organization: Nutrition and Integrative Neurobiology, INRA UMR 1286, University of Bordeaux, Department of Neuroscience, Columbia University
– sequence: 4
  givenname: H D
  surname: Vishwasrao
  fullname: Vishwasrao, H D
  organization: Department of Neuroscience, Columbia University
– sequence: 5
  givenname: D
  surname: Biezonski
  fullname: Biezonski, D
  organization: Departments of Psychiatry and Pharmacology, College of Physicians and Surgeons, Columbia University
– sequence: 6
  givenname: J
  surname: Mészáros
  fullname: Mészáros, J
  organization: Departments of Psychiatry and Pharmacology, College of Physicians and Surgeons, Columbia University
– sequence: 7
  givenname: E
  surname: Urizar
  fullname: Urizar, E
  organization: Departments of Psychiatry and Pharmacology, College of Physicians and Surgeons, Columbia University
– sequence: 8
  givenname: D R
  surname: Sibley
  fullname: Sibley, D R
  organization: Molecular Neuropharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health
– sequence: 9
  givenname: C
  surname: Kellendonk
  fullname: Kellendonk, C
  organization: Departments of Psychiatry and Pharmacology, College of Physicians and Surgeons, Columbia University, Division of Molecular Therapeutics, New York State Psychiatric Institute
– sequence: 10
  givenname: K C
  surname: Sonntag
  fullname: Sonntag, K C
  organization: Department of Psychiatry, McLean Hospital, Harvard Medical School
– sequence: 11
  givenname: D L
  surname: Graham
  fullname: Graham, D L
  organization: Department of Pharmacology, Vanderbilt University School of Medicine
– sequence: 12
  givenname: R J
  surname: Colbran
  fullname: Colbran, R J
  organization: Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Vanderbilt Kennedy Center and Vanderbilt Brain Institute, Vanderbilt University School of Medicine
– sequence: 13
  givenname: G D
  surname: Stanwood
  fullname: Stanwood, G D
  organization: Department of Pharmacology, Vanderbilt University School of Medicine, Vanderbilt Kennedy Center and Vanderbilt Brain Institute, Vanderbilt University School of Medicine
– sequence: 14
  givenname: J A
  surname: Javitch
  fullname: Javitch, J A
  email: gregg.stanwood@vanderbilt.edu, jaj2@columbia.edu
  organization: Departments of Psychiatry and Pharmacology, College of Physicians and Surgeons, Columbia University, Division of Molecular Therapeutics, New York State Psychiatric Institute
BackLink https://www.ncbi.nlm.nih.gov/pubmed/25560761$$D View this record in MEDLINE/PubMed
https://hal.inrae.fr/hal-02636137$$DView record in HAL
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Snippet Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation, because their purported potential to manifest signaling and...
Hetero-oligomers of G-protein-coupled receptors have become the subject of intense investigation because their purported potential to manifest signaling and...
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SubjectTerms 13/51
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine - analogs & derivatives
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine - pharmacology
42/44
631/378
64/60
9/10
96/33
Animals
Behavioral Sciences
Biological Psychology
Bioluminescence
Biosensors
Brain slice preparation
Corpus Striatum - drug effects
Corpus Striatum - metabolism
Depression, Mental
Dopamine
Dopamine Agonists - pharmacology
Dopamine Antagonists - pharmacology
Dopamine D1 receptors
Dopamine D2 receptors
Dopamine receptors
Drug therapy
G protein-coupled receptors
Grooming
Grooming - drug effects
GTP-Binding Protein alpha Subunits, Gq-G11 - genetics
GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism
HEK293 Cells
Humans
Kinases
Life Sciences
Ligands
Localization
Luminescent Proteins - genetics
Luminescent Proteins - metabolism
Male
Medicine
Medicine & Public Health
Mental disorders
Mice
Mice, Inbred C57BL
Mice, Knockout
Models, Molecular
Motor Activity - drug effects
Motor Activity - genetics
Mutants
Neurosciences
Nucleus accumbens
Nucleus Accumbens - drug effects
Nucleus Accumbens - metabolism
Oligomers
original-article
Pharmacology
Pharmacotherapy
Phospholipase C
Phosphorylation - drug effects
Physiological aspects
Protein Multimerization - drug effects
Protein Multimerization - physiology
Protein Structure, Tertiary
Proteins
Psychiatry
Receptor mechanisms
Receptors, Dopamine D1 - genetics
Receptors, Dopamine D1 - metabolism
Receptors, Dopamine D2 - genetics
Receptors, Dopamine D2 - metabolism
Risk factors
Schizophrenia
Signal transduction
Title Evidence against dopamine D1/D2 receptor heteromers
URI https://link.springer.com/article/10.1038/mp.2014.166
https://www.ncbi.nlm.nih.gov/pubmed/25560761
https://www.proquest.com/docview/1724253832
https://www.proquest.com/docview/2331618557
https://www.proquest.com/docview/1725522458
https://www.proquest.com/docview/1765953774
https://hal.inrae.fr/hal-02636137
https://pubmed.ncbi.nlm.nih.gov/PMC4492915
Volume 20
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