ArticlePloS one2015
Conantokin-G attenuates detrimental effects of NMDAR hyperactivity in an ischemic rat model of stroke.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
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- A new class of peptides from wasp venom: a pathway to antiepileptic/neuroprotective drugs.Brain communications · 2023Article
- Effects of Treadmill Exercise on Social Behavior in Rats Exposed to Thimerosal with Respect to the Hippocampal Level of GluN1, GluN2A, and GluN2B.Journal of molecular neuroscience : MN · 2022Article
- Intermittent Hypoxia Activates N-Methyl-D-Aspartate Receptors to Induce Anxiety Behaviors in a Mouse Model of Sleep-Associated Apnea.Molecular neurobiology · 2021Article
- Hormone-like conopeptides - new tools for pharmaceutical design.RSC medicinal chemistry · 2020Review
- Transcriptomic Profiling Reveals Extraordinary Diversity of Venom Peptides in Unexplored Predatory Gastropods of the Genus Clavus.Genome biology and evolution · 2020Article
- The three-dimensional structure of an H-superfamily conotoxin reveals a granulin fold arising from a common ICK cysteine framework.The Journal of biological chemistry · 2019Article
- Exercise training increases spatial memory via reducing contralateral hippocampal NMDAR subunits expression in intracerebral hemorrhage rats.Neuropsychiatric disease and treatment · 2019Article
- Bioactive Compounds Isolated from Neglected Predatory Marine Gastropods.Marine drugs · 2018Review
- GLYX-13, a NMDA Receptor Glycine-Site Functional Partial Agonist, Attenuates Cerebral Ischemia InjuryFrontiers in aging neuroscience · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The neuroprotective activity of conantokin-G (con-G), a naturally occurring antagonist of N-methyl-D-aspartate receptors (NMDAR), was neurologically and histologically compared in the core and peri-infarct regions after ischemia/reperfusion brain injury in male Sprague-Dawley rats. The contralateral regions served as robust internal controls. Intrathecal injection of con-G, post-middle carotid artery occlusion (MCAO), caused a dramatic decrease in brain infarct size and swelling at 4 hr, compared to 26 hr, and significant recovery of neurological deficits was observed at 26 hr. Administration of con-G facilitated neuronal recovery in the peri-infarct regions as observed by decreased neurodegeneration and diminished calcium microdeposits at 4 hr and 26 hr. Intact Microtubule Associated Protein (MAP2) staining and neuronal cytoarchitecture was observed in the peri-infarct regions of con-G treated rats at both timepoints. Con-G restored localization of GluN1 and GluN2B subunits in the neuronal soma, but not that of GluN2A, which was perinuclear in the peri-infarct regions at 4 hr and 26 hr. This suggests that molecular targeting of the GluN2B subunit has potential for reducing detrimental consequences of ischemia. Overall, the data demonstrated that stroke-induced NMDAR excitoxicity is ameliorated by con-G-mediated repair of neurological and neuroarchitectural deficits, as well as by reconstituting neuronal localization of GluN1 and GluN2B subunits in the peri-infarct region of the stroked brain.
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