ArticleFrontiers in neuroanatomy2011
Identification of a specific assembly of the g protein golf as a critical and regulated module of dopamine and adenosine-activated cAMP pathways in the striatum.
Article in Frontiers in neuroanatomy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- The Signaling and Pharmacology of the Dopamine D1 Receptor.Frontiers in cellular neuroscience · 2021Pooled it
- Modulation of striatal cAMP levels: A key pathway in the treatment of hyperkinetic movement disorders.iScience · 2026Article
- Dopaminergic Inhibition of the Inwardly Rectifying Potassium Current in Direct Pathway Medium Spiny Neurons in Normal and Parkinsonian Striatum.Brain sciences · 2025Article
- Molecular Imbalances Between Striosome and Matrix Compartments Characterize the Pathogenesis and Pathophysiology of Huntington's Disease Model Mouse.International journal of molecular sciences · 2025Article
- Mouse Gnal transcripts and transcriptomics in isolated dystonia.Research square · 2025Article
- Characterization of GαiScience · 2025Article
- Spiking Patterns in the Globus Pallidus Highlight Convergent Neural Dynamics across Diverse Genetic Dystonia Syndromes.Annals of neurology · 2025Article
- A humanized Gs-coupled DREADD for circuit and behavior modulation.Frontiers in cellular neuroscience · 2025Article
- Adenosine receptor subtype modulators: Insight into molecular mechanisms and their therapeutic application.American journal of translational research · 2025Review
- Brain network pathophysiology in dystonia.Dystonia (Lausanne, Switzerland) · 2025Article
- DYT-Frontiers in neuroscience · 2023Review
- Phosphodiesterase 10A (PDE10A): Regulator of Dopamine Agonist-Induced Gene Expression in the Striatum.Cells · 2022Article
- Functional abnormalities in the cerebello-thalamic pathways in a mouse model of DYT25 dystonia.eLife · 2022Article
- G protein-coupled receptor-effector macromolecular membrane assemblies (GEMMAs).Pharmacology & therapeutics · 2022Review
- Motor, epileptic, and developmental phenotypes in genetic disorders affecting G protein coupled receptors-cAMP signaling.Frontiers in neurology · 2022Review
- Forsythoside A Mitigates Alzheimer's-like Pathology by Inhibiting Ferroptosis-mediated Neuroinflammation via Nrf2/GPX4 Axis Activation.International journal of biological sciences · 2022Article
- Small Non-coding RNAs Are Dysregulated in Huntington's Disease Transgenic Mice Independently of the Therapeutic Effects of an Environmental Intervention.Molecular neurobiology · 2021Article
- Emerging and converging molecular mechanisms in dystonia.Journal of neural transmission (Vienna, Austria : 1996) · 2021Review
- cAMP-Fyn signaling in the dorsomedial striatum direct pathway drives excessive alcohol use.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- The mammalian target of rapamycin (mTOR) kinase mediates haloperidol-induced cataleptic behavior.Translational psychiatry · 2020Article
3 more citing papers are in PubMed but not listed here.
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1 author at 1 institution in 1 country.
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Abstract
In the principal neurons of striatum (medium spiny neurons, MSNs), cAMP pathway is primarily activated through the stimulation of dopamine D1 and adenosine A(2A) receptors, these receptors being mainly expressed in striatonigral and striatopallidal MSNs, respectively. Since cAMP signaling pathway could be altered in various physiological and pathological circumstances, including drug addiction and Parkinson's disease, it is of crucial importance to identify the molecular components involved in the activation of this pathway. In MSNs, cAMP pathway activation is not dependent on the classical Gs GTP-binding protein but requires a specific G protein subunit heterotrimer containing Gαolf/β2/γ7 in particular association with adenylyl cyclase type 5. This assembly forms an authentic functional signaling unit since loss of one of its members leads to defects of cAMP pathway activation in response to D1 or A(2A) receptor stimulation, inducing dramatic impairments of behavioral responses dependent on these receptors. Interestingly, D1 receptor (D1R)-dependent cAMP signaling is modulated by the neuronal levels of Gαolf, indicating that Gαolf represents the rate-limiting step in this signaling cascade and could constitute a critical element for regulation of D1R responses. In both Parkinsonian patients and several animal models of Parkinson's disease, the lesion of dopamine neurons produces a prolonged elevation of Gαolf levels. This observation gives an explanation for the cAMP pathway hypersensitivity to D1R stimulation, occurring despite an unaltered D1R density. In conclusion, alterations in the highly specialized assembly of Gαolf/β2/γ7 subunits can happen in pathological conditions, such as Parkinson's disease, and it could have important functional consequences in relation to changes in D1R signaling in the striatum.
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