The use of cerebral blood flow as an index of neuronal activity in functional neuroimaging: experimental and pathophysiological considerations

2000 ◽  
Vol 20 (3-4) ◽  
pp. 215-224 ◽  
Author(s):  
Willy Gsell ◽  
Christelle De Sadeleer ◽  
Yannick Marchalant ◽  
Eric T. MacKenzie ◽  
Pascale Schumann ◽  
...  
2020 ◽  
Vol 376 (1815) ◽  
pp. 20190622
Author(s):  
Anusha Mishra ◽  
Catherine N. Hall ◽  
Clare Howarth ◽  
Ralph D. Freeman

Functional neuroimaging using MRI relies on measurements of blood oxygen level-dependent (BOLD) signals from which inferences are made about the underlying neuronal activity. This is possible because neuronal activity elicits increases in blood flow via neurovascular coupling, which gives rise to the BOLD signal. Hence, an accurate interpretation of what BOLD signals mean in terms of neural activity depends on a full understanding of the mechanisms that underlie the measured signal, including neurovascular and neurometabolic coupling, the contribution of different cell types to local signalling, and regional differences in these mechanisms. Furthermore, the contributions of systemic functions to cerebral blood flow may vary with ageing, disease and arousal states, with regard to both neuronal and vascular function. In addition, recent developments in non-invasive imaging technology, such as high-field fMRI, and comparative inter-species analysis, allow connections between non-invasive data and mechanistic knowledge gained from invasive cellular-level studies. Considered together, these factors have immense potential to improve BOLD signal interpretation and bring us closer to the ultimate purpose of decoding the mechanisms of human cognition. This theme issue covers a range of recent advances in these topics, providing a multidisciplinary scientific and technical framework for future work in the neurovascular and cognitive sciences. This article is part of the theme issue ‘Key relationships between non-invasive functional neuroimaging and the underlying neuronal activity'.


2018 ◽  
Vol 11 ◽  
Author(s):  
Manami Takahashi ◽  
Takuya Urushihata ◽  
Hiroyuki Takuwa ◽  
Kazumi Sakata ◽  
Yuhei Takado ◽  
...  

2015 ◽  
Vol 114 (3) ◽  
pp. 1353-1356 ◽  
Author(s):  
Mauro DiNuzzo

Extensive research over the past decades about the multifaceted roles of brain astrocytes led to the suggestion that the signals observed with functional neuroimaging might primarily reflect astrocytic rather than neuronal activity. The basis for this paradigm-shifting concept was the evidence for an involvement of astrocytes in the control of local cerebral blood flow through intracellular Ca2+ signaling. In this Neuro Forum, I discuss new important experimental findings obtained by Jego et al. (Jego P, Pacheco-Torres J, Araque A, Canals S. J Cereb Blood Flow Metab 34: 1599–1603, 2014) as well as other closely related studies published recently, prompting a dismissal of substantial astrocytic contribution in functional neuroimaging.


2015 ◽  
Vol 35 (6) ◽  
pp. 883-887 ◽  
Author(s):  
Francisco Fernandez-Klett ◽  
Josef Priller

Pericytes are mural cells with contractile properties. Here, we provide evidence that microvascular pericytes modulate cerebral blood flow in response to neuronal activity (‘functional hyperemia’). Besides their role in neurovascular coupling, pericytes are responsive to brain damage. Cerebral ischemia is associated with constrictions and death of capillary pericytes, followed by fibrotic reorganization of the ischemic tissue. The data suggest that precapillary arterioles and capillaries are major sites of hemodynamic regulation in the brain.


2012 ◽  
Vol 302 (5) ◽  
pp. H1185-H1194 ◽  
Author(s):  
Julian M. Stewart ◽  
Marvin S. Medow ◽  
Zachary R. Messer ◽  
Ila L. Baugham ◽  
Courtney Terilli ◽  
...  

Neurocognition is impaired in chronic fatigue syndrome (CFS). We propose that the impairment relates to postural cerebral hemodynamics. Twenty-five CFS subjects and twenty control subjects underwent incremental upright tilt at 0, 15, 30, 45, 60, and 75° with continuous measurement of arterial blood pressure and cerebral blood flow velocity (CBFV). We used an n-back task with n ranging from 0 to 4 (increased n = increased task difficulty) to test working memory and information processing. We measured n-back outcomes by the number of correct answers and by reaction time. We measured CBFV, critical closing pressure (CCP), and CBFV altered by neuronal activity (activated CBFV) during each n value and every tilt angle using transcranial Doppler ultrasound. N-back outcome in control subjects decreased with n valve but was independent of tilt angle. N-back outcome in CFS subjects decreased with n value but deteriorated as orthostasis progressed. Absolute mean CBFV was slightly less than in control subjects in CFS subject at each angle. Activated CBFV in control subjects was independent of tilt angle and increased with n value. In contrast, activated CBFV averaged 0 in CFS subjects, decreased with angle, and was less than in control subjects. CCP was increased in CFS subjects, suggesting increased vasomotor tone and decreased metabolic control of CBFV. CCP did not change with orthostasis in CFS subjects but decreased monotonically in control subjects, consistent with vasodilation as compensation for the orthostatic reduction of cerebral perfusion pressure. Increasing orthostatic stress impairs neurocognition in CFS subjects. CBFV activation, normally tightly linked to cognitive neuronal activity, is unrelated to cognitive performance in CFS subjects; the increased CCP and vasomotor tone may indicate an uncoupling of the neurovascular unit during orthostasis.


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