Relevant bibliographies by topics / Neurovascular coupling (NVC)

Academic literature on the topic 'Neurovascular coupling (NVC)'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Neurovascular coupling (NVC)"

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Teskey, G. Campbell, and Cam Ha T. Tran. "Neurovascular Coupling in Seizures." Neuroglia 2, no. 1 (October 11, 2021): 36–47. http://dx.doi.org/10.3390/neuroglia2010005.

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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.
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Balbi, Matilde, Masayo Koide, George C. Wellman, and Nikolaus Plesnila. "Inversion of neurovascular coupling after subarachnoid hemorrhage in vivo." Journal of Cerebral Blood Flow & Metabolism 37, no. 11 (January 23, 2017): 3625–34. http://dx.doi.org/10.1177/0271678x16686595.

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Subarachnoid hemorrhage (SAH) induces acute changes in the cerebral microcirculation. Recent findings ex vivo suggest neurovascular coupling (NVC), the process that increases cerebral blood flow upon neuronal activity, is also impaired after SAH. The aim of the current study was to investigate whether this occurs also in vivo. C57BL/6 mice were subjected to either sham surgery or SAH by filament perforation. Twenty-four hours later NVC was tested by forepaw stimulation and CO2 reactivity by inhalation of 10% CO2. Vessel diameter was assessed in vivo by two-photon microscopy. NVC was also investigated ex vivo using brain slices. Cerebral arterioles of sham-operated mice dilated to 130% of baseline upon CO2 inhalation or forepaw stimulation and cerebral blood flow (CBF) increased. Following SAH, however, CO2 reactivity was completely lost and the majority of cerebral arterioles showed paradoxical constriction in vivo and ex vivo resulting in a reduced CBF response. As previous results showed intact NVC 3 h after SAH, the current findings indicate that impairment of NVC after cerebral hemorrhage occurs secondarily and is progressive. Since neuronal activity-induced vasoconstriction (inverse NVC) is likely to further aggravate SAH-induced cerebral ischemia and subsequent brain damage, inverse NVC may represent a novel therapeutic target after SAH.
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Sundqvist, Nicolas, Sebastian Sten, Peter Thompson, Benjamin Jan Andersson, Maria Engström, and Gunnar Cedersund. "Mechanistic model for human brain metabolism and its connection to the neurovascular coupling." PLOS Computational Biology 18, no. 12 (December 22, 2022): e1010798. http://dx.doi.org/10.1371/journal.pcbi.1010798.

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The neurovascular and neurometabolic couplings (NVC and NMC) connect cerebral activity, blood flow, and metabolism. This interconnection is used in for instance functional imaging, which analyses the blood-oxygen-dependent (BOLD) signal. The mechanisms underlying the NVC are complex, which warrants a model-based analysis of data. We have previously developed a mechanistically detailed model for the NVC, and others have proposed detailed models for cerebral metabolism. However, existing metabolic models are still not fully utilizing available magnetic resonance spectroscopy (MRS) data and are not connected to detailed models for NVC. Therefore, we herein present a new model that integrates mechanistic modelling of both MRS and BOLD data. The metabolic model covers central metabolism, using a minimal set of interactions, and can describe time-series data for glucose, lactate, aspartate, and glutamate, measured after visual stimuli. Statistical tests confirm that the model can describe both estimation data and predict independent validation data, not used for model training. The interconnected NVC model can simultaneously describe BOLD data and can be used to predict expected metabolic responses in experiments where metabolism has not been measured. This model is a step towards a useful and mechanistically detailed model for cerebral blood flow and metabolism, with potential applications in both basic research and clinical applications.
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Toth, Adam Nyul, Tabea Wiedenhoeft, Stefano Tarantini, Tamas Csipo, Priya Balasubramanian, Anna Csiszar, Agnes Csiszar, and Zoltan Ungvari. "Fusogenic Liposomes Deliver Resveratrol to Brain Microcirculation and Improve Neurovascular Coupling in Aged Mice." Innovation in Aging 4, Supplement_1 (December 1, 2020): 120. http://dx.doi.org/10.1093/geroni/igaa057.394.

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Abstract Adjustment of cerebral blood flow (CBF) to the increased oxygen and nutrient demands of active brain regions via neurovascular coupling (NVC) has an essential role in maintenance of healthy cognitive function. In advanced age, cerebromicrovascular oxidative stress and endothelial dysfunction impair neurovascular coupling, contributing to age-related cognitive decline. Recently we developed a resveratrol (3,4′,5- trihydroxystilbene)-containing fusogenic liposome (FL-RSV)-based molecular delivery system that can effectively target cultured cerebromicrovascular endothelial cells, attenuating age-related oxidative stress. To assess the cerebromicrovascular protective effects of FL-RSV in vivo, aged (24-monthold) C57BL/6 mice were treated with FL-RSV for four days. To demonstrate effective cellular uptake of FL-RSV, accumulation of the lipophilic tracer dyes in cells of the neurovascular unit was confirmed using two-photon imaging (through a chronic cranial window). NVC was assessed by measuring CBF responses (laser speckle contrast imaging) evoked by contralateral whisker stimulation. We found that NVC responses were significantly impaired in aged mice. Treatment with FL-RSV significantly improved NVC responses by increasing NO-mediated vasodilation. These findings are paralleled by the protective effects of FL-RSV on endothelium-dependent relaxation in the aorta. Thus, treatment with FL-RSV rescues endothelial function and NVC responses in aged mice. We propose that resveratrol containing fusogenic liposomes could also be used for combined delivery of various anti-geronic factors, including proteins, small molecules, DNA vectors and mRNAs targeting key pathways involved in microvascular aging and neurovascular dysfunction for the prevention/treatment of age-related cerebromicrovascular pathologies and development of vascular cognitive impairment (VCI) in aging.
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Lefferts, Wesley K., William E. Hughes, Corey N. White, Tom D. Brutsaert, and Kevin S. Heffernan. "Effect of acute nitrate supplementation on neurovascular coupling and cognitive performance in hypoxia." Applied Physiology, Nutrition, and Metabolism 41, no. 2 (February 2016): 133–41. http://dx.doi.org/10.1139/apnm-2015-0400.

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The matching of oxygen supply to neural demand (i.e., neurovascular coupling (NVC)) is an important determinant of cognitive performance. The impact of hypoxia on NVC remains poorly characterized. NVC is partially modulated by nitric oxide (NO), which may initially decrease in hypoxia. This study investigated the effect of acute NO-donor (nitrate) supplementation on NVC and cognitive function in hypoxia. Twenty healthy men participated in this randomized, double-blind, crossover design study. Following normoxic cognitive/NVC testing, participants consumed either nitrate (NIT) or a NIT-depleted placebo (PLA). Participants then underwent 120 min of hypoxia (11.6% ± 0.1% O2) and all cognitive/NVC testing was repeated. NVC was assessed as change in middle cerebral artery (MCA) blood flow during a cognitive task (incongruent Stroop) using transcranial Doppler. Additional computerized cognitive testing was conducted separately to assess memory, executive function, attention, sensorimotor, and social cognition domains. Salivary nitrite significantly increased following supplementation in hypoxia for NIT (+2.6 ± 1.0 arbitrary units (AU)) compared with PLA (+0.2 ± 0.3 AU; p < 0.05). Memory performance (−6 ± 13 correct) significantly decreased (p < 0.05) in hypoxia while all other cognitive domains were unchanged in hypoxia for both PLA and NIT conditions (p > 0.05). MCA flow increased during Stroop similarly in normoxia (PLA +5 ± 6 cm·s−1, NIT +7 ± 7 cm·s−1) and hypoxia (PLA +5 ± 9 cm·s−1, NIT +6 ± 7 cm·s−1) (p < 0.05) and this increase was not altered by PLA or NIT (p > 0.05). In conclusion, acute hypoxia resulted in significant reductions in memory concomitant with preservation of executive function, attention, and sensorimotor function. Hypoxia had no effect on NVC. Acute NIT supplementation had no effect on NVC or cognitive performance in hypoxia.
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Kirton, Adam, Carolyn Gunraj, and Robert Chen. "TMS Neuro-Cardiovascular Coupling in Vascular Compression Cranial Neuropathy." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 36, no. 1 (January 2009): 83–88. http://dx.doi.org/10.1017/s0317167100006363.

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Background:Neurovascular compression (NVC) may cause cranial mononeuropathy but lacks a definitive diagnostic investigation. We hypothesized that the arterial pressure wave (APW) would interact at the neurovascular interface in NVC to inhibit transmission of transcranial magnetic stimulation (TMS) stimuli to affected muscles.Methods:We report a novel neurophysiological method coupling cardiovascular physiology with TMS. The electrocardiogram (ECG) and arterial pressure wave (APW) were coupled to triggering of cortical TMS in a patient with NVC-induced spinal accessory (CNXI) mononeuropathy. Outcome measures included motor evoked potential (MEP) amplitudes and firing probabilities of normal and affected trapezieus (TPZ). Values at intervals in proximity to the APW (40/80/120/160ms) were compared to baseline (800ms) using ANOVA and student t-test.Results:Electrocardiogram triggered TMS of CNXI pathways with 100% reliability. MEP amplitudes were decreased in proximity to the APW, particularly at 120ms (0.21±0.04 mV versus 0.39±0.10mV, p=0.003). TPZ firing probabilities were similarly inhibited (43.8% versus 88.2%, p=0.009). No effect of APW proximity was observed on the unaffected side (p=0.868). Procedures were well tolerated.Conclusions:Vascular compression causes CNXI mononeuropathy. Transcranial magnetic stimulation-cardiovascular coupling may evaluate neurovascular junction interactions and non-invasively diagnose NVC.
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Csipo, Tamas, Agnes Lipecz, Peter Mukli, Dhay Bahadli, Osamah Abdulhussein, Cameron D. Owens, Stefano Tarantini, et al. "Increased cognitive workload evokes greater neurovascular coupling responses in healthy young adults." PLOS ONE 16, no. 5 (May 19, 2021): e0250043. http://dx.doi.org/10.1371/journal.pone.0250043.

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Understanding how the brain allocates resources to match the demands of active neurons under physiological conditions is critically important. Increased metabolic demands of active brain regions are matched with hemodynamic responses known as neurovascular coupling (NVC). Several methods that allow noninvasive assessment of brain activity in humans detect NVC and early detection of NVC impairment may serve as an early marker of cognitive impairment. Therefore, non-invasive NVC assessments may serve as a valuable tool to detect early signs of cognitive impairment and dementia. Working memory tasks are routinely employed in the evaluation of cognitive task-evoked NVC responses. However, recent attempts that utilized functional near-infrared spectroscopy (fNIRS) or transcranial Doppler sonography (TCD) while using a similar working memory paradigm did not provide convincing evidence for the correlation of the hemodynamic variables measured by these two methods. In the current study, we aimed to compare fNIRS and TCD in their performance of differentiating NVC responses evoked by different levels of working memory workload during the same working memory task used as cognitive stimulation. Fourteen healthy young individuals were recruited for this study and performed an n-back cognitive test during TCD and fNIRS monitoring. During TCD monitoring, the middle cerebral artery (MCA) flow was bilaterally increased during the task associated with greater cognitive effort. fNIRS also detected significantly increased activation during a more challenging task in the left dorsolateral prefrontal cortex (DLPFC), and in addition, widespread activation of the medial prefrontal cortex (mPFC) was also revealed. Robust changes in prefrontal cortex hemodynamics may explain the profound change in MCA blood flow during the same cognitive task. Overall, our data support our hypothesis that both TCD and fNIRS methods can discriminate NVC evoked by higher demand tasks compared to baseline or lower demand tasks.
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Anfray, Antoine, Antoine Drieu, Vincent Hingot, Yannick Hommet, Mervé Yetim, Marina Rubio, Thomas Deffieux, Mickael Tanter, Cyrille Orset, and Denis Vivien. "Circulating tPA contributes to neurovascular coupling by a mechanism involving the endothelial NMDA receptors." Journal of Cerebral Blood Flow & Metabolism 40, no. 10 (October 30, 2019): 2038–54. http://dx.doi.org/10.1177/0271678x19883599.

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The increase of cerebral blood flow evoked by neuronal activity is essential to ensure enough energy supply to the brain. In the neurovascular unit, endothelial cells are ideally placed to regulate key neurovascular functions of the brain. Nevertheless, some outstanding questions remain about their exact role neurovascular coupling (NVC). Here, we postulated that the tissue-type plasminogen activator (tPA) present in the circulation might contribute to NVC by a mechanism dependent of its interaction with endothelial N-Methyl-D-Aspartate Receptor (NMDAR). To address this question, we used pharmacological and genetic approaches to interfere with vascular tPA-dependent NMDAR signaling, combined with laser speckle flowmetry, intravital microscopy and ultrafast functional ultrasound in vivo imaging. We found that the tPA present in the blood circulation is capable of potentiating the cerebral blood flow increase induced by the activation of the mouse somatosensorial cortex, and that this effect is mediated by a tPA-dependent activation of NMDAR expressed at the luminal part of endothelial cells of arteries. Although blood molecules, such as acetylcholine, bradykinin or ATP are known to regulate vascular tone and induce vessel dilation, our present data provide the first evidence that circulating tPA is capable of influencing neurovascular coupling (NVC).
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Tarantini, Stefano, Andriy Yabluchanskiy, Praveen Ballabh, Eszter Farkas, Joseph Baur, David Sinclair, Anna Csiszar, and Zoltan Ungvari. "NMN Rescues Endothelial Function and Neurovascular Coupling, Improving Cognitive Function in Aged Mice." Innovation in Aging 4, Supplement_1 (December 1, 2020): 121. http://dx.doi.org/10.1093/geroni/igaa057.399.

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Abstract Adjustment of cerebral blood flow (CBF) to neuronal activity via neurovascular coupling (NVC) has an essential role in maintenance of healthy cognitive function. In aging increased oxidative stress and cerebromicrovascular endothelial dysfunction impair NVC, contributing to cognitive decline. There is increasing evidence showing that a decrease in NAD+ availability with age plays a critical role in a range of age-related cellular impairments but its role in impaired NVC responses remains unexplored. The present study was designed to test the hypothesis that restoring NAD+ concentration may exert beneficial effects on NVC responses in aging. To test this hypothesis 24-month-old C57BL/6 mice were treated with nicotinamide mononucleotide (NMN), a key NAD+ intermediate, for 2 weeks. NVC was assessed by measuring CBF responses (laser Doppler flowmetry) evoked by contralateral whisker stimulation. We found that NVC responses were significantly impaired in aged mice. NMN supplementation rescued NVC responses by increasing endothelial NO-mediated vasodilation, which was associated with significantly improved spatial working memory and gait coordination. These findings are paralleled by the sirtuin-dependent protective effects of NMN on mitochondrial production of reactive oxygen species and mitochondrial bioenergetics in cultured cerebromicrovascular endothelial cells derived from aged animals. Thus, a decrease in NAD+ availability contributes to age-related cerebromicrovascular dysfunction, exacerbating cognitive decline. The cerebromicrovascular protective effects of NMN highlight the preventive and therapeutic potential of NAD+ intermediates as effective interventions in patients at risk for vascular cognitive impairment (VCI).
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Samora, Milena, Lauro C. Vianna, Jake C. Carmo, Victor Macedo, Matthew Dawes, Aaron A. Phillips, Julian F. R. Paton, and James P. Fisher. "Neurovascular coupling is not influenced by lower body negative pressure in humans." American Journal of Physiology-Heart and Circulatory Physiology 319, no. 1 (July 1, 2020): H22—H31. http://dx.doi.org/10.1152/ajpheart.00076.2020.

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Visual stimulation evoked a robust increase in posterior cerebral artery velocity and a modest increase in vertebral artery blood flow, i.e., neurovascular coupling (NVC), which was unaffected by lower body negative pressure in humans (LBNP). In addition, although LBNP induced a mild hypocapnia, this degree of hypocapnia in the absence of LBNP failed to modify the NVC response.
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Book chapters on the topic "Neurovascular coupling (NVC)"

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Kenney, Kimbra, Margalit Haber, and Ramon Diaz-Arrastia. "Traumatic Cerebral Vascular Injury." In Neurotrauma, edited by Kentaro Shimoda, Shoji Yokobori, and Ross Bullock, 55–68. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190279431.003.0006.

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Traumatic cerebral vascular injury (TCVI) is a frequent, if not universal, feature after traumatic brain injury (TBI). Because multiple pharmacologic and nonpharmacologic therapies promote vascular health, TCVI is an attractive target for therapeutic intervention after TBI. The cerebral microvasculature is a component of the neurovascular unit (NVU) coupling neuronal metabolism with local cerebral blood flow. The NVU participates in the pathogenesis of TBI, either directly from physical trauma or as part of the cascade of secondary injury that occurs after TBI. Pathologically, there is extensive microvascular injury in humans and experimental animals, identified with either conventional light microscopy or ultrastructural examination. Noninvasive, physiologic measures of cerebral microvascular function show dysfunction after TBI in humans and experimental animal models of TBI. These include imaging sequences, transcranial Doppler, and near infrared spectroscopy. Understanding the pathophysiology of TCVI, a relatively understudied component of TBI, has promise for the development of novel therapies for TBI.
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Conference papers on the topic "Neurovascular coupling (NVC)"

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Das, Yudhajit, Hanli Liu, Fenghua Tian, Yu-Lun Liu, Srinivas Kota, Rong Zhang, and Lina F. Chalak. "Neurovascular Coupling (NVC) in Newborns based on regional cerebral tissue oxygenation and amplitude EEG." In Clinical and Translational Biophotonics. Washington, D.C.: OSA, 2020. http://dx.doi.org/10.1364/translational.2020.jtu3a.25.

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