ArticleJournal of computational neuroscience2018
The role of astrocytic calcium and TRPV4 channels in neurovascular coupling.
Article in Journal of computational neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- Calcium Buffering in Astrocytes and Its Relevance for Experimental Data Interpretation and Computational Modeling.Journal of neurochemistry · 2026Review
- Systems biology analysis of vasodynamics in mouse cerebral arterioles during resting state and functional hyperemia.PLoS computational biology · 2026Article
- Activity driven sleep dynamics: A conceptual modeling study.PloS one · 2026Article
- Nitric oxide is not responsible for initial sensory-induced neurovascular coupling response in the barrel cortex of lightly anesthetized mice.Neurophotonics · 2025Article
- A computational framework for quantifying blood flow dynamics across myogenically-active cerebral arterial networks.Biomechanics and modeling in mechanobiology · 2025Article
- Modeling of Blood Flow Dynamics in Rat Somatosensory Cortex.Biomedicines · 2024Article
- Review
- Astrocytes: new evidence, new models, new roles.Biophysical reviews · 2023Review
- Astrocytic TRPV4 Channels and Their Role in Brain Ischemia.International journal of molecular sciences · 2023Review
- The Reversal Characteristics of GABAergic Neurons: A Neurovascular Model.Journal of biomechanical engineering · 2023Article
- Modeling the heterogeneity of sodium and calcium homeostasis between cortical and hippocampal astrocytes and its impact on bioenergetics.Frontiers in cellular neuroscience · 2023Article
- Grey-box modeling and hypothesis testing of functional near-infrared spectroscopy-based cerebrovascular reactivity to anodal high-definition tDCS in healthy humans.PLoS computational biology · 2021Article
- Transient Receptor Potential Vanilloid in the Brain Gliovascular Unit: Prospective Targets in Therapy.Pharmaceutics · 2021Review
- In-depth quantitative proteomic characterization of organotypic hippocampal slice culture reveals sex-specific differences in biochemical pathways.Scientific reports · 2021Article
- Astroglial Modulation of Hydromineral Balance and Cerebral Edema.Frontiers in molecular neuroscience · 2018Review
- Article
- Computational Models for Calcium-Mediated Astrocyte Functions.Frontiers in computational neuroscience · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal activity evokes a localised change in cerebral blood flow in a response known as neurovascular coupling (NVC). Although NVC has been widely studied the exact mechanisms that mediate this response remain unclear; in particular the role of astrocytic calcium is controversial. Mathematical modelling can be a useful tool for investigating the contribution of various signalling pathways towards NVC and for analysing the underlying cellular mechanisms. The lumped parameter model of a neurovascular unit with both potassium and nitric oxide (NO) signalling pathways and comprised of neurons, astrocytes, and vascular cells has been extended to include the glutamate induced astrocytic calcium pathway with epoxyeicosatrienoic acid (EET) signalling and the stretch dependent TRPV4 calcium channel on the astrocytic endfoot. Results show that the potassium pathway governs the fast onset of vasodilation while the NO pathway has a delayed response, maintaining dilation longer following neuronal stimulation. Increases in astrocytic calcium concentration via the calcium signalling pathway and/or TRPV4 channel to levels consistent with experimental data are insufficient for inducing either vasodilation or constriction, in contrast to a number of experimental results. It is shown that the astrocyte must depolarise in order to produce a significant potassium flux through the astrocytic BK channel. However astrocytic calcium is shown to strengthen potassium induced NVC by opening the BK channel further, consequently allowing more potassium into the perivascular space. The overall effect is vasodilation with a higher maximal vessel radius.
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