ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Signaling from blood vessels to CNS axons through nitric oxide.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 62 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
62 citing papers in PubMed, 122 citations in OpenAlex.
- Neurovascular coupling in the basolateral amygdala modulates negative emotions.Cell research · 2026Article
- Psychedelic 5-HTNature neuroscience · 2025Article
- Cerebrovascular-mediated dynamic alterations in neurovascular coupling: a key pathological mechanism of depression.Cell & bioscience · 2025Review
- Neural Metabolic Networks: Key Elements of Healthy Brain Function.Journal of neurochemistry · 2025Review
- Cognitive Impairment and Synaptic Dysfunction in Cardiovascular Disorders: The New Frontiers of the Heart-Brain Axis.Biomedicines · 2024Review
- The Unexpected Role of the Endothelial Nitric Oxide Synthase at the Neurovascular Unit: Beyond the Regulation of Cerebral Blood Flow.International journal of molecular sciences · 2024Review
- Anoxia-induced hippocampal LTP is regeneratively produced by glutamate and nitric oxide from the neuro-glial-endothelial axis.iScience · 2024Article
- Constitutive NOS Production Is Modulated by Alzheimer's Disease Pathology Depending on APOE Genotype.International journal of molecular sciences · 2024Article
- Article
- Towards modifying the genetic predisposition for glaucoma: An overview of the contribution and interaction of genetic and environmental factors.Molecular aspects of medicine · 2023Review
- Intravenous administration of apeling-13 induces a depressor response by releasing an unidentified substance.Biochemical and biophysical research communications · 2023Article
- Review
- Could respiration-driven blood oxygen changes modulate neural activity?Pflugers Archiv : European journal of physiology · 2023Review
- Neurovascular coupling: motive unknown.Trends in neurosciences · 2022Review
- Toward an integrative neurovascular framework for studying brain networks.Neurophotonics · 2022Article
- Deficiency of Endothelial Nitric Oxide Synthase (eNOS) Exacerbates Brain Damage and Cognitive Deficit in A Mouse Model of Vascular Dementia.Aging and disease · 2021Article
- Aerobic Glycolysis in the Brain: Warburg and Crabtree Contra Pasteur.Neurochemical research · 2021Review
- N-Methyl-D-aspartate Glutamate Receptor Modulates Cardiovascular and Neuroendocrine Responses Evoked by Hemorrhagic Shock in Rats.BioMed research international · 2021Article
- Nitric oxide signalling in the brain and its control of bodily functions.British journal of pharmacology · 2020Review
- Spatial and temporal patterns of nitric oxide diffusion and degradation drive emergent cerebrovascular dynamics.PLoS computational biology · 2020Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedKollb-Sielecka, Martha [corrected to Kollb-Sielecka, Marta]
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Brain function is usually perceived as being performed by neurons with the support of glial cells, the network of blood vessels situated nearby serving simply to provide nutrient and to dispose of metabolic waste. Revising this view, we find from experiments on a rodent central white matter tract (the optic nerve) in vitro that microvascular endothelial cells signal persistently to axons using nitric oxide (NO) derived from the endothelial NO synthase (eNOS). The endogenous NO acts to stimulate guanylyl cyclase-coupled NO receptors in the axons, leading to a raised cGMP level which then causes membrane depolarization, apparently by directly engaging hyperpolarization-activated cyclic nucleotide-gated ion channels. The tonic depolarization and associated endogenous NO-dependent cGMP generation was absent in optic nerves from mice lacking eNOS, although such nerves responded to exogenous NO, with raised cGMP generation in the axons and associated depolarization. In addition to the tonic activity, exposure of optic nerves to bradykinin, a classical stimulator of eNOS in endothelial cells, elicited reversible NO- and cGMP-dependent depolarization through activation of bradykinin B2 receptors, to which eNOS is physically complexed. No contribution of other NO synthase isoforms to either the action of bradykinin or the continuous ambient NO level could be detected. The results suggest that microvascular endothelial cells participate in signal processing in the brain and can do so by generating both tonic and phasic NO signals.
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What OpenQuestion holds
Registered trials
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.