ArticlePurinergic signalling2013
Reduced striatal ecto-nucleotidase activity in schizophrenia patients supports the "adenosine hypothesis".
Article in Purinergic signalling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- The Role of Purine Metabolism and Uric Acid in Postnatal Neurologic Development.Molecules (Basel, Switzerland) · 2025Review
- Article
- Ectonucleotidase Activity in Smooth Muscle Tissues of Rats with a Valproate Model of Autism.Bulletin of experimental biology and medicine · 2024Article
- The adenosine hypothesis of schizophrenia into its third decade: From neurochemical imbalance to early life etiological risks.Frontiers in cellular neuroscience · 2023Review
- Altered purinergic receptor expression in the frontal cortex in schizophrenia.Schizophrenia (Heidelberg, Germany) · 2022Article
- Adenosine, Schizophrenia and Cancer: Does the Purinergic System Offer a Pathway to Treatment?International journal of molecular sciences · 2022Review
- Enzyme histochemistry: a useful tool for examining the spatial distribution of brain ectonucleotidases in (patho)physiological conditions.Histology and histopathology · 2022Review
- Adenosine Receptors in Neuropsychiatric Disorders: Fine Regulators of Neurotransmission and Potential Therapeutic Targets.International journal of molecular sciences · 2022Review
- Adenosine Kinase Expression in the Frontal Cortex in Schizophrenia.Schizophrenia bulletin · 2020Article
- Role of Ectonucleotidases in Synapse Formation During Brain Development: Physiological and Pathological Implications.Current neuropharmacology · 2019Review
- Alterations of Astrocytes in the Context of Schizophrenic Dementia.Frontiers in pharmacology · 2019Review
- Purine-related metabolites and their converting enzymes are altered in frontal, parietal and temporal cortex at early stages of Alzheimer's disease pathology.Brain pathology (Zurich, Switzerland) · 2018Article
- Cell-subtype-specific changes in adenosine pathways in schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- Purinergic system in psychiatric diseases.Molecular psychiatry · 2018Review
- Deletion of adenosine A2A receptors from astrocytes disrupts glutamate homeostasis leading to psychomotor and cognitive impairment: relevance to schizophrenia.Biological psychiatry · 2015Article
- Comorbidities in Neurology: Is adenosine the common link?Neuropharmacology · 2015Review
- High expression of ecto-nucleotidases CD39 and CD73 in human endometrial tumors.Mediators of inflammation · 2014Article
- Purinergic Receptors of the Central Nervous System: Biology, PET Ligands, and Their Applications.Molecular imagingReview
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schizophrenia (SZ) is a major chronic neuropsychiatric disorder characterized by a hyperdopaminergic state. The hypoadenosinergic hypothesis proposes that reduced extracellular adenosine levels contribute to dopamine D2 receptor hyperactivity. ATP, through the action of ecto-nucleotidases, constitutes a main source of extracellular adenosine. In the present study, we examined the activity of ecto-nucleotidases (NTPDases, ecto-5'-nucleotidase, and alkaline phosphatase) in the postmortem putamen of SZ patients (n = 13) compared with aged-matched controls (n = 10). We firstly demonstrated, by means of artificial postmortem delay experiments, that ecto-nucleotidase activity in human brains was stable up to 24 h, indicating the reliability of this tissue for these enzyme determinations. Remarkably, NTPDase-attributable activity (both ATPase and ADPase) was found to be reduced in SZ patients, while ecto-5'-nucleotidase and alkaline phosphatase activity remained unchanged. In the present study, we also describe the localization of these ecto-enzymes in human putamen control samples, showing differential expression in blood vessels, neurons, and glial cells. In conclusion, reduced striatal NTPDase activity may contribute to the pathophysiology of SZ, and it represents a potential mechanism of adenosine signalling impairment in this illness.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.