ArticleNeurobiology of disease2012
The NMDA receptor co-agonists, D-serine and glycine, regulate neuronal dendritic architecture in the somatosensory cortex.
Article in Neurobiology of disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 97 citations in OpenAlex.
- Novel drug treatments for schizophrenia.Nature reviews. Drug discovery · 2026Review
- Derivatization agents for LC-MS analysis of amino acids: effects of core structure and functional groups.Analytical and bioanalytical chemistry · 2026Article
- Impact of D-Amino Acids in Schizophrenia.Biomolecules · 2025Review
- Neural Metabolic Networks: Key Elements of Healthy Brain Function.Journal of neurochemistry · 2025Review
- Dysfunction of the NMDA Receptor in the Pathophysiology of Schizophrenia and/or the Pathomechanisms of Treatment-Resistant Schizophrenia.Biomolecules · 2024Review
- Subcortical control of the default mode network: Role of the basal forebrain and implications for neuropsychiatric disorders.Brain research bulletin · 2022Review
- Article
- Glycine-induced NMDA receptor internalization provides neuroprotection and preserves vasculature following ischemic stroke.iScience · 2022Article
- D-cysteine is an endogenous regulator of neural progenitor cell dynamics in the mammalian brain.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Increased excitation-inhibition balance and loss of GABAergic synapses in the serine racemase knockout model of NMDA receptor hypofunction.Journal of neurophysiology · 2021Article
- Forebrain expression of serine racemase during postnatal development.Neurochemistry international · 2021Article
- Altered neural oscillations and behavior in a genetic mouse model of NMDA receptor hypofunction.Scientific reports · 2021Article
- Fifty Years of Research on Schizophrenia: The Ascendance of the Glutamatergic Synapse.The American journal of psychiatry · 2020Review
- Positive allosteric modulators that target NMDA receptors rectify loss-of-function GRIN variants associated with neurological and neuropsychiatric disorders.Neuropharmacology · 2020Article
- D-Serine as the gatekeeper of NMDA receptor activity: implications for the pharmacologic management of anxiety disorders.Translational psychiatry · 2020Review
- Translational neurophysiological biomarkers of N-methyl-d-aspartate receptor dysfunction in serine racemase knockout mice.Biomarkers in neuropsychiatry · 2020Article
- Neurotoxic astrocytes express the d-serine synthesizing enzyme, serine racemase, in Alzheimer's disease.Neurobiology of disease · 2019Article
- Sociality deficits in serine racemase knockout mice.Brain and behavior · 2019Article
- Administration of memantine reverses behavioral, histological, and electrophysiological abnormalities in rats subjected to early maternal deprivation.Journal of neural transmission (Vienna, Austria : 1996) · 2019Article
- Dendritic Spine Elimination: Molecular Mechanisms and Implications.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2019Review
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5 authors at 2 institutions in 1 country.
Funding
Abstract
There is substantial evidence, both pharmacological and genetic, that hypofunction of the N-methyl-d-aspartate receptor (NMDAR) is a core pathophysiological feature of schizophrenia. There are morphological brain changes associated with schizophrenia, including perturbations in the dendritic morphology of cortical pyramidal neurons and reduction in cortical volume. Our experiments investigated whether these changes in dendritic morphology could be recapitulated in a genetic model of NMDAR hypofunction, the serine racemase knockout (SR-/-) mouse. Pyramidal neurons in primary somatosensory cortex (S1) of SR-/- mice had reductions in the complexity, total length, and spine density of apical and basal dendrites. In accordance with reduced cortical neuropil, SR-/- mice also had reduced cortical volume as compared to wild type mice. Analysis of S1 mRNA by DNA microarray and gene expression analysis revealed gene changes in SR-/- that are associated with psychiatric and neurologic disorders, as well as neurodevelopment. The microarray analysis also identified reduced expression of brain derived neurotrophic factor (BDNF) in SR-/- mice. Follow-up analysis by ELISA confirmed a reduction of BDNF protein levels in the S1 of SR-/- mice. Finally, S1 pyramidal neurons in glycine transporter heterozygote (GlyT1+/-) mutants, which display enhanced NMDAR function, had increased dendritic spine density. These results suggest that proper NMDAR function is important for the arborization and spine density of pyramidal neurons in cortex. Moreover, they suggest that NMDAR hypofunction might, in part, be contributing to the dendritic and synaptic changes observed in schizophrenia and highlight this signaling pathway as a potential target for therapeutic intervention.
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