Fig 1.
The chemical exchange saturation transfer (CEST) effect of γ-aminobutyric acid (GABA) and its dependence on the B1 amplitude.
(a) Image of a phantom with 50 mM GABA (pH, 7.0) and the localization voxel indicated. (b, c) Z-spectra and CEST asymmetry curves for 50 mM GABA (pH, 7.0) at different B1 amplitudes show the CEST effect at approximately 2.75 ppm downfield to the bulk water resonance. (d) The CEST effect of GABA increases with an increase in the B1 amplitude and remains steady after the B1 amplitude reaches 6.0 μT.
Fig 2.
Chemical exchange saturation transfer (CEST) images of a phantom comprising test tubes with different concentrations of γ-aminobutyric acid (GABA) solutions (pH, 7.0) immersed in a beaker containing phosphate-buffered saline (PBS).
(a) The region of interest (ROI) shows the CEST contrast color-coded on the original CEST image (2.75 ppm) acquired by the application of a saturation continuous wave with a B1 amplitude of 6.0 μT (255 Hz) for 5 s. (b) Linear dependence of the CEST effect of GABA on the GABA concentration, with a slope of 0.58% mM−.
Fig 3.
Chemical exchange saturation transfer (CEST) images of a phantom comprising test tubes with solutions containing 50 mM of different metabolites [γ-aminobutyric acid (GABA), glutamine (Gln), myoinositol (MI), creatinine (Cr), and choline (Cho)] at a peak B1 amplitude of 6 μT (255 Hz) and a 5-s saturation pulse duration.
Except for some contribution from Glu, there was no apparent contribution from the other metabolites at 2.75 ppm.
Fig 4.
Images of a rat brain with a tumor and disrupted blood—brain barrier (BBB).
(a) T2-weighted image demonstrating the tumor and a rectangular region of interest. (b) Chemical exchange saturation transfer (CEST) maps of γ-aminobutyric acid (GABA) in a rat brain with a tumor and a compromised BBB, which were collected at baseline and 50 min, 1.5 h, and 2.0 h after GABA injection, show a gradual increase in the CEST effect of GABA over time.