Amino acids related to neurotransmitters and the GABAergic/glutamatergic system were measured using a 3 T-MRI instrument in 12 patients with autism and 10 normal controls. All measurements were performed in the frontal lobe (FL) and lenticular nuclei (LN) using a conventional sequence for n-acetyl aspartate (NAA) and glutamate (Glu), and the MEGA-editing method for GABA. The GABA level and [GABA]/[NAA] ratio were significantly lower (p < 0.01) in the FL, but not the LN, in patients with autism compared to normal controls. The [GABA]/[Glu] ratio in the FL was also significantly lower (p < 0.05) in the patients than in the normal controls, thus suggesting a possible abnormality in the regulation between GABA and Glu.
The objectives of this study were to examine the reproducibility of the MEGA-editing J-difference technique and to determine the normal variation in the γ-aminobutyric acid (GABA) level depending on the cerebral region and its fluctuation according to the menstrual cycle as baseline data for clinical application. The participants consisted of 15 normal adult volunteers (eight men and seven women), and all measurements were repeated twice in all participants. The MEGA-editing pulses were incorporated into point-resolved spectroscopy on a 3 T instrument to obtain the J-difference editing spectra from a voxel located in the lentiform nuclei (LN), left frontal lobe (FL), and anterior cingulate cortex (AC). The GABA levels in the gray matter (GM) were compensated by the fraction ratios of the gray and white matters and cerebrospinal fluid in the measurement volume. The extent of the variation in GABA was almost the same as that observed in the major metabolites, and its reproducibility was also maintained (intraclass correlation coefficient > 0.7). GABA level was highest in LN and lowest in AC. A difference in the GABA level between the follicular and luteal phases of the menstrual cycle was found in both LN and FL, but not in AC. This technique showed the differences in the GABA levels in the GM and the region-specific decrease in the GABA levels during the women's luteal phase.
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