One of those coupling mechanisms involves glutamate released for synaptic activation, which induces a change in Ca +2 in neighboring astrocytes. Furthermore, the vascular response is also coupled very tightly. It is obvious that the metabolic load change is coupled directly to the neuronal activation. The coupling to synaptic activity is very tight. This means that fMRI reflects the synaptic activity driving neuronal assemblies, but cannot disclose the information content of the neuronal firing patterns produced by the neurons. The neuronal processes causing BOLD signal changes are associated with synaptic inputs at the site of activation, not with the output level of firing of the neuron receiving synaptic inputs (Logothetis et al 2001). The neural basis of BOLD signals and neuro-vascular coupling \) Then the positive BOLD signal (\(\Delta Y > 0\)) requires that \(\Delta CMRglu/CMRglu > \Delta CMRO2/CMRO2\) and the energy metabolism during neural activation has to be less oxidative.
The change in the glucose consumption and CBF upon neural activation has been reported to be \(\Delta CMRglu/CMRglu =\Delta CBF/CBF\ ,\) where \(CMRx\) is the cerebral metabolic rate of \(x\. The energy metabolism of the brain is known to be highly oxidative at the resting state, using glucose as the carbon source. This situation corresponds to the case when \(\Delta CBF/CBF\) is larger than the fractional oxygen extraction change and the corresponding BOLD signal increases. Therefore, OEF decreases (more oxygen supply than the consumption) make \(\Delta Y\) positive. The BOLD effect is related to changes in physiological conditions (Ogawa et al, 1998) and appears as a part of the relaxation rate \(1/T_2^*\. The measurement was only possible during the time window when the agent passed through areas of interest in the brain.īOLD MR image signal and its relation to physiology Prior to these reports, another fMRI method for detection of a functional response in the human brain was published in 1991 (Belliveau et al 1991), using an exogenous contrast agent injected into the blood stream. The era of BOLD-based functional MRI (using the endogenous contrast agent, deoxyhemoglobin) started with three papers that appeared in 1992 (Bandettini et al 1992, Kwong et al 1992, Ogawa et al 1992) (see Raichle 2000 for a historical perspective on fMRI development). It should be noted that Thulborn et al showed, in their in vitro blood experiments, that blood water T2 varies with deoxyhemoglobin content (Thulborn et al 1982). The image intensity that varies with deoxyhemoglobin content has been termed Blood Oxygenation Level Dependent (BOLD) and was suggested for potential use in functional study of the brain by Ogawa et al (1990). When the content of deoxyhemoglobin changes in the blood, the relaxation process of water protons is modified and one can see these changes in MRI. Water protons in these areas sense these field distortions, which are reflected in the signal decay process, characterized by T2 (spin echo) or T2*(gradient echo) relaxation. In the large homogenous magnetic fields used in MRI, compartmentalized susceptibility differences induce small magnetic field distortions in the blood as well as in the surrounding extra-vascular area. The presence of deoxyhemoglobin in red blood cells makes their magnetic susceptibility different from the diamagnetic plasma in blood and, similarly, induces a difference in magnetic susceptibility between the blood and the surrounding tissue. In contrast, oxygen-bound hemoglobin, oxyhemoglobin, has low spin (S = 0) and is diamagnetic (Pauling & Coryl 1936). Hemoglobin without bound oxygen molecules, deoxyhemoglobin, is paramagnetic because of the high spin state (S = 2) of the heme iron. 4 Activation maps and functional networksīOLD based fMRI method BOLD effects in MR images.3 Low frequency oscillation of fMRI signal and spontaneous activity at rest.1.5 Advantages and disadvantages of BOLD fMRI.1.3 The neural basis of BOLD signals and neuro-vascular coupling.1.2 BOLD MR image signal and its relation to physiology.
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