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Glutamatergic synapse in autism: a complex story for a complex disorder
Laurent Galineau1, Nicolas Arlicot1,2, Anne-Claire Dupont1,2,3
1UMR 1253, iBrain, Université de Tours, Inserm, Tours, France.
Molecular Psychiatry
|November 26, 2022
Summary
Autism spectrum disorder (ASD) involves complex glutamate system changes. Research found increased mGluR5 density in adults with ASD, suggesting it reflects adaptation rather than a primary cause.
Area of Science:
- Neuroscience
- Biochemistry
- Medical Imaging
Background:
- Autism spectrum disorder (ASD) pathophysiology remains unclear, with debated roles for glutamate system dysfunction.
- Previous studies on brain and peripheral glutamate levels in ASD yielded inconsistent results, leading to competing hypotheses.
- Emerging research suggests elevated metabotropic glutamate receptor 5 (mGluR5) densities may be implicated in ASD.
Purpose of the Study:
- To investigate glutamate dysfunctions in adults with ASD.
- To quantify glutamate levels in the cingulate cortex and periphery.
- To assess mGluR5 brain density in adults with ASD and in a valproate-induced animal model of ASD.
Main Methods:
- Proton magnetic resonance spectroscopy and metabolomics were used to measure glutamate levels.
- Positron emission tomography (PET) was employed to quantify mGluR5 brain density.
- A valproic acid-induced prenatal exposure rat model was used to study developmental changes.
Main Results:
- No significant differences in cingulate cortex glutamate levels were found between individuals with ASD and controls.
- Adults with ASD exhibited an overall increased density of mGluR5 in the brain.
- In the animal model, increased mGluR5 density was observed primarily subcortically in adolescent rats, but not in the childhood-equivalent stage.
Conclusions:
- Cingulate cortex glutamate levels do not appear significantly altered in adults with ASD, highlighting challenges in assessing excitatory transmission via spectroscopy.
- Increased mGluR5 density in adults with ASD may represent an adaptive response to earlier glutamatergic alterations.
- mGluR5 density changes might reflect compensatory mechanisms rather than being a primary driver of ASD pathophysiology.
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