Targeted NMDA receptor interventions for autism: developmentally determined expression of GluN2B and GluN2A-containing receptors and balanced allosteric modulatory approaches
Open accessAbstract
Various ASD risk alleles have been associated with impairment of NMDA receptor activation (i.e., NMDA Receptor Hypofunction) and/or disturbance of the careful balance between activation mediated by GluN2B-subtype and GluN2A-subtype-containing NMDA receptors. Importantly, although these various risk alleles affect NMDA receptor activation through different mechanisms, they share the pathogenic consequences of causing disturbance of highly regulated NMDA receptor activation. Disturbances of NMDA receptor activation due to sequence variants, protein termination variants and copy number variants are often cell-specific and regionally selective. Thus, translational therapeutic NMDA receptor agonist interventions, which may require chronic administration, must have specificity, selectivity and facilitate NMDA receptor activation in a manner that is physiologic (i.e., mimicking that of endogenously released glutamate and glycine/D-serine released in response to salient and relevant socio-cognitive provocations within discrete neural circuits). Importantly, knockout mice with absent expression and mice with haploinsufficient expression of the deleterious genes often serve as good models to test the potential efficacy of promising pharmacotherapeutic strategies. The Review considers diverse examples of “illness” genes, their pathogenic effects on NMDA receptor activation and, when available, results of studies of impaired sociability in mouse models, including “proof of principle/proof of concept” experiments exploring NMDA receptor agonist interventions and the development of promising positive allosteric modulators (PAMs), which serve as support and models for developing an inventory of PAMs and negative allosteric modulators (NAMs) for translational therapeutic intervention. Conceivably, selective PAMs and NAMs either alone or in combination will be administered to patients guided by their genotype in order to potentiate and/or restore disrupted balance between activation mediated by GluN2B-subtype and GluN2A-subtype containing NMDA receptors.
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Rare, often de novo, missense or truncating variants in GRIN1, GRIN2A, GRIN2B, and GRIA2 alter receptor kinetics, calcium signaling, and synaptic strength, and have been implicated in ASD.
“Rare, often de novo, missense or truncating variants in these genes alter receptor kinetics, calcium signaling, and synaptic strength, and have been implicated in ASD (Deutsch et al., 2022; Sheng et al., 2022; Gjerulfsen et al., 2024).”
From Biological hierarchy from genotype to phenotype in syndromic and non-syndromic autism spectrum disorder (2026) · cites this paper as Deutsch et al., 2022
Section 2.3 (page unavailable) reports rare, de novo missense variants in GRIN1, GRIN2A and GRIN2B in patients, some with autistic features, and describes effects on receptor deactivation and calcium permeability. The Introduction mentions protein-termination variants generally, but our copy does not establish the full claim for truncating variants, GRIA2, calcium signaling or synaptic strength. (LLM, conf=0.88)
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“Rare, often de novo , missense or truncating variants in these genes alter receptor kinetics, calcium signaling, and synaptic strength, and have been implicated in ASD (Deutsch et al., 2022; Sheng et al., 2022; Gjerulfsen et al., 2024).”
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- Authors
- Deutsch, S. I., Luyo, Z. N. M., & Burket, J. A.
- Affiliations
- Eastern Virginia Medical School (US)
- Christopher Newport University (US)
- Corresponding author
- Burket, Jessica A.
- Venue
- Biomolecules
- Publisher
- MDPI AG
- Published
- 2022-01-22
- Volume
- 12
- Issue
- 2
- Pages
- 181
- ISSN
- 2218-273X (ISSN-L)
- PMC
- PMC8961601
- OpenAlex
- W4214690840
- Cited by
- 22
- References
- 68
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 4 · 2023: 5 · 2022: 4
- FWCI
- 0.68
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Biomolecules (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Keywords
- NMDA receptor hypofunction, autism spectrum disorder, GluN2B, GluN2A, positive allosteric modulators, negative allosteric modulators, NMDA receptor agonist, copy number variation, haploinsufficiency, knockout mouse models, sociability
- MeSH terms
- Animals, Autistic Disorder, Humans, Signal Transduction, Receptors, N-Methyl-D-Aspartate, Mice, Knockout, Glutamic Acid, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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