ArticleInternational journal of molecular sciences2019
Role of Neuron⁻Glia Signaling in Regulation of Retinal Vascular Tone in Rats.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Retinal Neurovascular Coupling: From Mechanisms to a Diagnostic Window into Brain Disorders.Cells · 2025Review
- Retinal TRP channels: Cell-type-specific regulators of retinal homeostasis and multimodal integration.Progress in retinal and eye research · 2023Review
- Oxidative stress in the brain and retina after traumatic injury.Frontiers in neuroscience · 2023Review
- Role of Prostaglandins in Nitric Oxide-Induced Glial Cell-Mediated Vasodilation in Rat Retina.Biomolecules · 2022Article
- L-Citrulline ameliorates the attenuation of acetylcholine-induced vasodilation of retinal arterioles in diabetic rats.Heliyon · 2021Article
- The "Neuro-Glial-Vascular" Unit: The Role of Glia in Neurovascular Unit Formation and Dysfunction.Frontiers in cell and developmental biology · 2021Review
- Retinal Physiology and Circulation: Effect of Diabetes.Comprehensive Physiology · 2020Review
- Retinal-glia ischemia and inflammation induced by chronic stress: The SABPA study.Brain, behavior, & immunity - health · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
The interactions between neuronal, glial, and vascular cells play a key role in regulating blood flow in the retina. In the present study, we examined the role of the interactions between neuronal and glial cells in regulating the retinal vascular tone in rats upon stimulation of retinal neuronal cells by intravitreal injection of N-methyl-d-aspartic acid (NMDA). The retinal vascular response was assessed by measuring the diameter of the retinal arterioles in the in vivo fundus images. Intravitreal injection of NMDA produced retinal vasodilation that was significantly diminished following the pharmacological inhibition of nitric oxide (NO) synthase (nNOS), loss of inner retinal neurons, or intravitreal injection of glial toxins. Immunohistochemistry revealed the expression of nNOS in ganglion and calretinin-positive amacrine cells. Moreover, glial toxins significantly prevented the retinal vasodilator response induced by intravitreal injection of NOR3, an NO donor. Mechanistic analysis revealed that NO enhanced the production of vasodilatory prostanoids and epoxyeicosatrienoic acids in glial cells in a ryanodine receptor type 1-dependent manner, subsequently inducing the retinal vasodilator response. These results suggest that the NO released from stimulated neuronal cells acts as a key messenger in neuron-glia signaling, thereby causing neuronal activity-dependent and glial cell-mediated vasodilation in the retina.
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Registered trials
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