Glutamine synthesis could underly the physiological inhibitory control of dopaminergic D1 receptor signals.
The enhanced glutamate-glutamine metabolism might be due to astroglial activation and the consequent reinforcement of glutamine synthesis in autistic brains. In autism and TD groups, ACC D1 receptor radioligand binding was negatively correlated with ACC glutamine levels (r = − 0.55, p = 0.022 r = − 0.58, p = 0.008, respectively). The autism group showed elevated glutamate, glutamine, and myo-inositol (mI) levels compared with the TD group ( p = 0.045, p = 0.044, p = 0.030, respectively) and a positive correlation between glutamine and mI levels in the ACC (r = 0.54, p = 0.020). We enrolled 18 male adults with high-functioning autism and 20 typically developed (TD) male subjects. We tested this hypothesis using magnetic resonance spectroscopy and positron emission tomography scan with 11C-SCH23390 for dopamine D1 receptors in the anterior cingulate cortex (ACC). The amplified glutamate signals may arise from enhanced glutamatergic circuits, which can be affected by astrocyte activation and suppressive signaling of dopamine neurotransmission.
Increased excitatory neuronal tones have been implicated in autism, but its mechanism remains elusive.
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