Special Issue "Dynamic Vascular-Glial-Neuronal Interactions in Health and Disease"

A special issue of Neuroglia (ISSN 2571-6980).

Deadline for manuscript submissions: closed (10 October 2021).

Special Issue Editor

Prof. Dr. Jessica Filosa
E-Mail Website
Guest Editor
Department of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA
Interests: neurovascular; arteriole; pressure; calcium; ion channels; cerebral blood flow; astrocyte; microglia; myogenic; hypertension
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Dynamic crosstalk interactions among components of the neurovascular unit (NVU) maintain brain homeostasis. Importantly, neural and glial-derived signals regulate cerebral blood flow and the energetic demands of the brain. Impairments in these key constitutive processes uncouple communication at the NVU, impair cerebral perfusion, increase inflammation, and lead to progressive neurodegeneration.

Efforts have been devoted to the understanding of both physiological and pathological intercellular crosstalk at the NVU. Physiological processes such as cerebral autoregulation, neurovascular coupling, and vasculo-neuronal coupling are common pathways used to understand the state of oxygen and glucose delivery to the brain. Notably, both intrinsic and extrinsic cellular mechanisms can differentially alter the functional integrity of the NVU. Poorly understood are the cell-specific signaling pathways, as well as the stimuli thresholds (i.e., ischemia, intravascular and intracranial pressures) by which certain conditions switch from physiology to pathology. In addition, the contribution of cardiovascular risk factors and glymphatic dysfunction on neurodegeneration, vascular dementia, and Alzheimer’s are current critical areas of research.

This Special Issue seeks papers related to how disease processes impact brain hemodynamics, perfusion, and metabolism. Highlights on the importance of brain region specificity, on circuit connectivity, as well as studies addressing the molecular mechanisms underlying cell-specific crosstalk in health and disease are welcome. 

Prof. Jessica Filosa
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Neuroglia is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurovascular coupling
  • neurovascular unit
  • astrogliosis
  • microgliosis
  • intercellular crosstalk
  • vascular function
  • ion channels
  • inflammation
  • blood–brain barrier integrity
  • calcium

Published Papers (2 papers)

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Research

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Article
Direct Deviations in Astrocyte Free Ca2+ Concentration Control Multiple Arteriole Tone States
Neuroglia 2021, 2(1), 48-56; https://0-doi-org.brum.beds.ac.uk/10.3390/neuroglia2010006 - 14 Oct 2021
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Abstract
Astrocytes elicit bidirectional control of microvascular diameter in acutely isolated brain slices through vasoconstriction and vasodilation pathways that can be differentially recruited via the free Ca2+ concentration in endfeet and/or the metabolic status of the tissue. However, the Ca2+-level hypothesis [...] Read more.
Astrocytes elicit bidirectional control of microvascular diameter in acutely isolated brain slices through vasoconstriction and vasodilation pathways that can be differentially recruited via the free Ca2+ concentration in endfeet and/or the metabolic status of the tissue. However, the Ca2+-level hypothesis has not been tested using direct manipulation. To overcome this, we used Ca2+-clamp whole-cell patching of peri-arteriole astrocytes to change astrocyte-free Ca2+ to different concentrations and examined the vascular response. We discovered that clamping Ca2+ at the approximate resting value (100 nM) had no impact on arteriole diameter in a pre-constricted arteriole. However, a moderate elevation to 250 nM elicited sustained vasodilation that was blocked by the COX-1 antagonist SC-560 (500 nM). The vasodilation to 250 nM Ca2+ was sensitive to the metabolic state, as it converted to vasoconstriction when oxygen tension was dramatically elevated. In normal oxygen, clamping astrocyte Ca2+ well above the resting level (750 nM) produced sustained vasoconstriction, which converted to vasodilation in the 20-HETE blocker HET0016 (1 μM). This response was fully blocked by the addition of SC-560 (500 nM), showing that 20-HETE-induced vasoconstriction dominated the dilatory action of COX-1. These data demonstrate that direct changes in astrocyte free Ca2+ can control multiple arteriole tone states through different mediators. Full article
(This article belongs to the Special Issue Dynamic Vascular-Glial-Neuronal Interactions in Health and Disease)
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Review

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Review
Neurovascular Coupling in Seizures
Neuroglia 2021, 2(1), 36-47; https://0-doi-org.brum.beds.ac.uk/10.3390/neuroglia2010005 - 11 Oct 2021
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Abstract
Neurovascular coupling is a key control mechanism in cerebral blood flow (CBF) regulation. Importantly, this process was demonstrated to be affected in several neurological disorders, including epilepsy. Neurovascular coupling (NVC) is the basis for functional brain imaging, such as PET, SPECT, fMRI, and [...] Read more.
Neurovascular coupling is a key control mechanism in cerebral blood flow (CBF) regulation. Importantly, this process was demonstrated to be affected in several neurological disorders, including epilepsy. Neurovascular coupling (NVC) is the basis for functional brain imaging, such as PET, SPECT, fMRI, and fNIRS, to assess and map neuronal activity, thus understanding NVC is critical to properly interpret functional imaging signals. However, hemodynamics, as assessed by these functional imaging techniques, continue to be used as a surrogate to map seizure activity; studies of NVC and cerebral blood flow control during and following seizures are rare. Recent studies have provided conflicting results, with some studies showing focal increases in CBF at the onset of a seizure while others show decreases. In this brief review article, we provide an overview of the current knowledge state of neurovascular coupling and discuss seizure-related alterations in neurovascular coupling and CBF control. Full article
(This article belongs to the Special Issue Dynamic Vascular-Glial-Neuronal Interactions in Health and Disease)
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