The importance of the negative blood-oxygenation-level-dependent (BOLD) response in the somatosensory cortex

2015 ◽  
Vol 26 (6) ◽  
pp. 647-653 ◽  
Author(s):  
Carsten M. Klingner ◽  
Stefan Brodoehl ◽  
Otto W. Witte

AbstractIn recent years, multiple studies have shown task-induced negative blood-oxygenation-level-dependent responses (NBRs) in multiple brain regions in humans and animals. Converging evidence suggests that task-induced NBRs can be interpreted in terms of decreased neuronal activity. However, the vascular and metabolic dynamics and functional importance of the NBR are highly debated. Here, we review studies investigating the origin and functional importance of the NBR, with special attention to the somatosensory cortex.

2018 ◽  
Vol 39 (11) ◽  
pp. 2295-2307 ◽  
Author(s):  
Miguel Martínez-Maestro ◽  
Christian Labadie ◽  
Harald E Möller

Dynamic metabolic changes were investigated by functional magnetic resonance spectroscopy (fMRS) during sustained stimulation of human primary visual cortex. Two established paradigms, consisting of either a full-field or a small-circle flickering checkerboard, were employed to generate wide-spread areas of positive or negative blood oxygenation level-dependent (BOLD) responses, respectively. Compared to baseline, the glutamate concentration increased by 5.3% ( p = 0.007) during activation and decreased by −3.8% ( p = 0.017) during deactivation. These changes were positively correlated with the amplitude of the BOLD response ( R = 0.60, p = 0.002) and probably reflect changes of tricarboxylic acid cycle activity. During deactivation, the glucose concentration decreased by −7.9% ( p = 0.025) presumably suggesting increased consumption or reduced glucose supply. Other findings included an increased concentration of glutathione (4.2%, p = 0.023) during deactivation and a negative correlation of glutathione and BOLD signal changes ( R = −0.49, p = 0.012) as well as positive correlations of aspartate ( R = 0.44, p = 0.035) and N-acetylaspartylglutamate ( R = 0.42, p = 0.035) baseline concentrations with the BOLD response. It remains to be shown in future work if the observed effects on glutamate and glucose levels deviate from the assumption of a direct link between glucose utilization and regulation of blood flow or support previous suggestions that the hemodynamic response is mainly driven by feedforward release of vasoactive messengers.


2002 ◽  
Vol 22 (9) ◽  
pp. 1042-1053 ◽  
Author(s):  
Eric R. Cohen ◽  
Kamil Ugurbil ◽  
Seong-Gi Kim

The effect of the basal cerebral blood flow (CBF) on both the magnitude and dynamics of the functional hemodynamic response in humans has not been fully investigated. Thus, the hemodynamic response to visual stimulation was measured using blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) in human subjects in a 7-T magnetic field under different basal conditions: hypocapnia, normocapnia, and hypercapnia. Hypercapnia was induced by inhalation of a 5% carbon dioxide gas mixture and hypocapnia was produced by hyperventilation. As the fMRI baseline signal increased linearly with expired CO2 from hypocapnic to hypercapnic levels, the magnitude of the BOLD response to visual stimulation decreased linearly. Measures of the dynamics of the visually evoked BOLD response (onset time, full-width-at-half-maximum, and time-to-peak) increased linearly with the basal fMRI signal and the end-tidal CO2 level. The basal CBF level, modulated by the arterial partial pressure of CO2, significantly affects both the magnitude and dynamics of the BOLD response induced by neural activity. These results suggest that caution should be exercised when comparing stimulus-induced fMRI responses under different physiologic or pharmacologic states.


2011 ◽  
Vol 106 (6) ◽  
pp. 3010-3018 ◽  
Author(s):  
Mauro DiNuzzo ◽  
Tommaso Gili ◽  
Bruno Maraviglia ◽  
Federico Giove

A consistent and prominent feature of brain functional magnetic resonance imaging (fMRI) data is the presence of low-frequency (<0.1 Hz) fluctuations of the blood oxygenation level-dependent (BOLD) signal that are thought to reflect spontaneous neuronal activity. In this report we provide modeling evidence that cyclic physiological activation of astroglial cells produces similar BOLD oscillations through a mechanism mediated by intracellular Ca2+ signaling. Specifically, neurotransmission induces pulses of Ca2+ concentration in astrocytes, resulting in increased cerebral perfusion and neuroactive transmitter release by these cells (i.e., gliotransmission), which in turn stimulates neuronal activity. Noticeably, the level of neuron-astrocyte cross talk regulates the periodic behavior of the Ca2+ wave-induced BOLD fluctuations. Our results suggest that the spontaneous ongoing activity of neuroglial networks is a potential source of the observed slow fMRI signal oscillations.


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