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1  cerebral blood flow to neuronal metabolism (neurovascular coupling).
2 associated with increased neuronal activity (neurovascular coupling).
3  one of the key players in coordinating this neurovascular coupling.
4 f this glial cell-K+ siphoning hypothesis of neurovascular coupling.
5  only indirectly, by way of hemodynamics and neurovascular coupling.
6 zed changes in blood flow, a response termed neurovascular coupling.
7  retina does not contribute significantly to neurovascular coupling.
8 nd may help to refine quantitative models of neurovascular coupling.
9  a longer time span and is less dependent on neurovascular coupling.
10 derstand temporal correlations that describe neurovascular coupling.
11 t release Ca(2+) from stores does not affect neurovascular coupling.
12 y visual cortex to investigate the limits of neurovascular coupling.
13 hese networks, over and above the effects on neurovascular coupling.
14 ishing astrocytes as potential regulators of neurovascular coupling.
15 ulation, endothelial-mediated signaling, and neurovascular coupling.
16 nge in cerebral blood flow, a process termed neurovascular coupling.
17 ggesting that pericytes could have a role in neurovascular coupling.
18 gs, as well as a more principled modeling of neurovascular coupling.
19 tigators to probe the role of capillaries in neurovascular coupling.
20 rlying neuronal activity by a process termed neurovascular coupling.
21 Roy and Sherrington, 1890), a process termed neurovascular coupling.
22 e been proposed to play a role in functional neurovascular coupling.
23 V4 channels are engaged in and contribute to neurovascular coupling.
24 endfoot microdomain and assess their role in neurovascular coupling.
25 e synthase is involved in astrocyte-mediated neurovascular coupling.
26 erent conditions of neuronal stimulation and neurovascular coupling.
27 ha, and ultimately lead to the impairment of neurovascular coupling.
28 rocytes, and arterioles-causing inversion of neurovascular coupling.
29 l and impose constraints on future models of neurovascular coupling.
30 stent reduction in CBF, but not the impaired neurovascular coupling after CSD.
31                       Furthermore, disturbed neurovascular coupling after stroke can confound hemodyn
32 tant vascular diseases, or medication on the neurovascular coupling and consequently the functional M
33 amic response is important for understanding neurovascular coupling and elucidating the physiological
34 mutase (CuZnSOD) prevented the alteration in neurovascular coupling and endothelium-dependent respons
35 altered calcium signaling that could disrupt neurovascular coupling and gliotransmission.
36 may regulate experience-dependent changes in neurovascular coupling and myelination.
37 ions of mural cells in vascular development, neurovascular coupling and neuropathology.
38 ron, a direction opposite to that of classic neurovascular coupling and referred to here as vasculo-n
39 ults indicate that glial cells contribute to neurovascular coupling and suggest that regulation of bl
40  nitrite were not enough to entirely restore neurovascular coupling and supra-physiological concentra
41 esponses to investigate cocaine's effects on neurovascular coupling and to differentiate its effects
42 d with release of arachidonic acid, impaired neurovascular coupling, and reduced cerebral blood flow
43 ms based on recent astrocyte-based models of neurovascular coupling are discussed.
44 001), indicating that cocaine did not affect neurovascular coupling at rest and that the reduction in
45   The investigation of mechanisms underlying neurovascular coupling at the capillary level requires a
46 red hippocampal cytoarchitectonics; impaired neurovascular coupling; attenuated prepulse inhibition (
47                                              Neurovascular coupling between resting-state neural acti
48  responses were not, suggesting differential neurovascular coupling between the two vasculatures.
49            According to the current model of neurovascular coupling, blood flow is controlled regiona
50           Astrocytes play a critical role in neurovascular coupling by providing a physical linkage f
51            Here, we reexamined their role in neurovascular coupling by selectively expressing a genet
52 both adults and neonates, and a reduction in neurovascular coupling could deprive active neurons of a
53 ked neuronal activity.SIGNIFICANCE STATEMENT Neurovascular coupling, defined as the tight relationshi
54                             We conclude that neurovascular coupling depends critically on anesthesia
55 nse, showing that the degree and polarity of neurovascular coupling depends on astrocytic endfoot Ca(
56                                              Neurovascular coupling describes the link between neuron
57 min after cocaine injection, indicating that neurovascular coupling during stimulation was temporaril
58               The data are consistent with a neurovascular coupling effect in the retina.
59 orts a conceptual shift in the mechanisms of neurovascular coupling, from a unidimensional process in
60             The involvement of astrocytes in neurovascular coupling has broad implications for the in
61          One widely recognized hypothesis of neurovascular coupling holds that glial cell depolarizat
62 mechanism is essential to preserving healthy neurovascular coupling; however, to our knowledge, no st
63 ral blood flow that range from physiological neurovascular coupling (hyperaemia) to pathological inve
64 transcriptional regulator of SEMA3E-mediated neurovascular coupling in a mouse model of oxygen-induce
65 sis, and activity-induced neurometabolic and neurovascular coupling in adult (6 months) and aged (12
66      Here we address this issue by examining neurovascular coupling in both ex vivo and in vivo rat r
67                Wavelet coherence analysis of neurovascular coupling in NE may identify infants at ris
68 transcriptional regulator of SEMA3E-mediated neurovascular coupling in pathological retinal angiogene
69 nd a suite of in vivo imaging tools to study neurovascular coupling in rat primary somatosensory cort
70 estigated the contribution of glial cells to neurovascular coupling in the acutely isolated mammalian
71 hyperglycemia has a detrimental influence on neurovascular coupling in the brain-an effect linked to
72 direct proportionality of volumetric spatial neurovascular coupling in the cerebral cortex.
73   Our study examines the association between neurovascular coupling in the middle cerebral artery and
74 Here, we investigate spatial correlations of neurovascular coupling in three dimensions, by applying
75 -dependent Ca(2+) signaling does not mediate neurovascular coupling in visual cortex of awake, lightl
76 gs demonstrate that hyperoxia does not alter neurovascular coupling in vivo, ensuring that active neu
77  hindered by uncertainty as to the nature of neurovascular coupling in young individuals.
78              Under nitroprusside infusion, a neurovascular-coupling inhibitor, the diffusion response
79 ystem, the olfactory glomerulus, to show how neurovascular coupling involves an elaborate dance betwe
80                                              Neurovascular coupling is a process through which neuron
81         Fundamental to the interpretation of neurovascular coupling is determining the neuronal activ
82  superiorly to the optic nerve suggests that neurovascular coupling is perturbed.
83               Although this response, termed neurovascular coupling, is widely used to monitor human
84 lity and consequences of conditions in which neurovascular coupling may be altered, including during
85                                              Neurovascular coupling may be involved in compensatory m
86                                 Inversion of neurovascular coupling may contribute to the decreased c
87              Our results suggest that intact neurovascular coupling may help preserve mobility in eld
88                           This suggests that neurovascular coupling mechanism is likely to contain a
89  may fail in situations interfering with the neurovascular coupling mechanisms (drugs, anesthesia).
90            Here, we review current candidate neurovascular coupling mechanisms and propose that previ
91 is needed for improving our understanding of neurovascular coupling mechanisms and the related measur
92 standing of the signalling events underlying neurovascular coupling mechanisms in the brain is a cruc
93 he effects of wakefulness reflect changes in neurovascular coupling, not in neural activity.
94                       The classical model of neurovascular coupling (NVC) implies that activity-depen
95                                              Neurovascular coupling (NVC) is the process whereby neur
96                             Physiologically, neurovascular coupling (NVC) matches focal increases in
97  a proof of concept study aiming to quantify neurovascular coupling (NVC) using wavelet analysis of t
98     They play an important role in mediating neurovascular coupling (NVC) via several astrocytic Ca(2
99           Here we report that stress impairs neurovascular coupling (NVC), the process that matches n
100 sodilatory prostaglandins play a key role in neurovascular coupling (NVC), the tight link between neu
101 d hemodynamics, a phenomenon referred to as "neurovascular coupling" (NVC).
102 , we determined whether pathological inverse neurovascular coupling occurred as a mechanism of second
103 concept from the current electrochemical and neurovascular coupling principles used for brain imaging
104 del that incorporates internalization into a neurovascular-coupling relationship.
105 overed capillaries control vasomotion during neurovascular coupling remains controversial.
106  regulation of cerebral blood flow (CBF) and neurovascular coupling remains, however, under debate.
107 ling lead to a switch in the polarity of the neurovascular coupling response from vasodilation to vas
108 t improvement in cerebral blood flow and the neurovascular coupling response, as well as increased ex
109 ies such as Alzheimer's disease, would alter neurovascular coupling responses to sensory stimulation.
110 erebrovascular reactivity and whisker-evoked neurovascular coupling responses were measured at end po
111 nt for the full expression of sensory-evoked neurovascular coupling responses.
112 in slices, 100% O(2) has been shown to alter neurovascular coupling, suppressing activity-dependent v
113  simultaneous PET/fMRI for investigations of neurovascular coupling that correlate neurochemistry wit
114 Ca(2+) signaling within the endfoot mediates neurovascular coupling; thus, these functional microdoma
115  three patients exhibited dynamic changes in neurovascular coupling to depolarizations throughout the
116  physiological concentration fully recovered neurovascular coupling to its original magnitude.
117              These results establish inverse neurovascular coupling to spreading depolarization as a
118                                         This neurovascular coupling underlies blood oxygen level-depe
119                            The mechanisms of neurovascular coupling underlying generation of BOLD fMR
120  its newly recognized precursor, nitrite, in neurovascular coupling using a well-established rat mode
121 sed to 14.5 (95% CI, 2.3-91.1; p = 0.004) if neurovascular coupling was also attenuated.
122                                              Neurovascular coupling was assessed in bilateral middle
123                                              Neurovascular coupling was attenuated in slow compared t
124                     Persistent disruption of neurovascular coupling was demonstrated by a loss of coh
125                                     Further, neurovascular coupling was intact in lightly sedated, re
126                                We found that neurovascular coupling was similar across states and tha
127 , indicating that although O(2) can modulate neurovascular coupling when raised sufficiently high, th
128 mic responses consistent with more efficient neurovascular coupling within the left DLPFC.

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