Neuroglia

Special Issue Editor

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

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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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9 pages, 4249 KiB

Open AccessArticle

Direct Deviations in Astrocyte Free Ca²⁺ Concentration Control Multiple Arteriole Tone States

by Jordan N. Haidey and Grant R. Gordon

Neuroglia 2021, 2(1), 48-56; https://doi.org/10.3390/neuroglia2010006 - 14 Oct 2021

Cited by 1 | Viewed by 2685

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 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

Jump to: Research

12 pages, 621 KiB

Open AccessReview

Neurovascular Coupling in Seizures

by G. Campbell Teskey and Cam Ha T. Tran

Neuroglia 2021, 2(1), 36-47; https://doi.org/10.3390/neuroglia2010005 - 11 Oct 2021

Cited by 1 | Viewed by 3110

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 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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