ArticleCerebral cortex (New York, N.Y. : 1991)2020
Disrupting nNOS-PSD95 Interaction Improves Neurological and Cognitive Recoveries after Traumatic Brain Injury.
Article in Cerebral cortex (New York, N.Y. : 1991), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- Brain nitric oxide and inflammation in chronic intermittent hypoxia: Contributors to cognitive impairment and hypertension.Brain, behavior, & immunity - health · 2025Review
- Unveiling the role of PSD95 phosphorylation after traumatic brain injury: insights from phosphoproteomic analysis.BMC neurology · 2025Article
- Metabolite classification through novel metabolomics framework reveals mechanism underlying the therapeutic effects of PSD95-nNOS blockade for post-stroke depression.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- Exploring the role of parthanatos in CNS injury: Molecular insights and therapeutic approaches.Journal of advanced research · 2025Review
- PKR Inhibitor C16 Regulates HIV-gp120 Induced Neuronal Injury and Cognitive Impairment in Vivo and in Vitro Models.Neurochemical research · 2025Article
- K739 is preferentially targeted over K725 in the deSUMOylation process of neuronal nitric oxide synthase.Frontiers in chemistry · 2025Article
- Enhanced Fyn-tau and NR2B-PSD95 interactions in epileptic foci in experimental models and human epilepsy.Brain communications · 2024Article
- Polarized benzene rings can promote the interaction between CaM and the CaMBD region of nNOS.Frontiers in molecular neuroscience · 2024Article
- Cerebral glucagon-like peptide-1 receptor activation alleviates traumatic brain injury by glymphatic system regulation in mice.CNS neuroscience & therapeutics · 2023Article
- nNOS and Neurological, Neuropsychiatric Disorders: A 20-Year Story.Neuroscience bulletin · 2023Review
- Enhancement of the liver's neuroprotective role ameliorates traumatic brain injury pathology.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Gamma frequency entrainment rescues cognitive impairment by decreasing postsynaptic transmission after traumatic brain injury.CNS neuroscience & therapeutics · 2023Article
- GluN2B-containing NMDARs in the mammalian brain: pharmacology, physiology, and pathology.Frontiers in molecular neuroscience · 2023Review
- Targeting neuronal nitric oxide synthase and the nitrergic system in post-traumatic stress disorder.Psychopharmacology · 2022Review
- Inhibition of PSD95-nNOS protein-protein interactions decreases morphine reward and relapse vulnerability in rats.Addiction biology · 2022Article
- Synaptamide Modulates Astroglial Activity in Mild Traumatic Brain Injury.Marine drugs · 2022Article
- Fabrication of multifunctional metal-organic frameworks nanoparticles via layer-by-layer self-assembly to efficiently discover PSD95-nNOS uncouplers for stroke treatment.Journal of nanobiotechnology · 2022Article
- SerpinA3N attenuates ischemic stroke injury by reducing apoptosis and neuroinflammation.CNS neuroscience & therapeutics · 2022Article
- Krüppel-like factor 7 attenuates hippocampal neuronal injury after traumatic brain injury.Neural regeneration research · 2022Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Excessive activation of N-methyl-D-aspartate receptors (NMDARs) and the resulting neuronal nitric oxide synthase (nNOS) activation plays a crucial role in the pathogenesis of traumatic brain injury (TBI). However, directly inhibiting NMDARs or nNOS produces adverse side effects because they play key physiological roles in the normal brain. Since interaction of nNOS-PSD95 is a key step in NMDAR-mediated excitotoxicity, we investigated whether disrupting nNOS-PSD95 interaction with ZL006, an inhibitor of nNOS-PSD95 interaction, attenuates NMDAR-mediated excitotoxicity. In cortical neuronal cultures, ZL006 treatment significantly reduced glutamate-induced neuronal death. In a mouse model of controlled cortical impact (CCI), administration of ZL006 (10 mg/kg, i.p.) at 30 min postinjury significantly inhibited nNOS-PSD95 interaction, reduced TUNEL- and phospho-p38-positive neurons in the motor cortex. ZL006 treatment also significantly reduced CCI-induced cortical expression of apoptotic markers active caspase-3, PARP-1, ratio of Bcl-2/Bax, and phosphorylated p38 MAPK (p-p38). Functionally, ZL006 treatment significantly improved neuroscores and sensorimotor performance, reduced somatosensory and motor deficits, reversed CCI-induced memory deficits, and attenuated cognitive impairment. Histologically, ZL006 treatment significantly reduced the brain lesion volume. These findings collectively suggest that blocking nNOS-PSD95 interaction represents an attractive strategy for ameliorating consequences of TBI and that its action is mediated via inhibiting neuronal apoptosis and p38 MAPK signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.