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Dynamic metabolic changes in human visual cortex in regions with positive and negative blood oxygenation level-dependent response

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Martínez-Maestro,  Miguel
Methods and Development Unit Nuclear Magnetic Resonance, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Möller,  Harald E.
Methods and Development Unit Nuclear Magnetic Resonance, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Citation

Martínez-Maestro, M., Labadie, C., & Möller, H. E. (2019). Dynamic metabolic changes in human visual cortex in regions with positive and negative blood oxygenation level-dependent response. Journal of Cerebral Blood Flow and Metabolism, 39(11), 2295-2307. doi:10.1177/0271678X18795426.


Cite as: https://hdl.handle.net/21.11116/0000-0002-11CA-7
Abstract
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.