Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

NR2B subunit exerts a critical role in postischemic synaptic plasticity.

Barbara Picconi1, Anna Tortiglione, Ilaria Barone

  • 1Laboratorio di Neurofisiologia, Fondazione Santa Lucia, Rome, Italy.

Stroke
|June 3, 2006
PubMed
Summary

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Titration Dynamics and Early Treatment Burden in Advanced Parkinson's Disease: A Multicenter Comparison of CSFLI and LCIG Infusion Therapies.

Movement disorders clinical practice·2025
Same author

Are we ready for a biological diagnosis of Parkinson's Disease?

Cell death & disease·2025
Same author

Endoscopic Treatment of Staple-Line Leaks After Sleeve Gastrectomy in Patients with Obesity: Which One is the Best Option, if Any? A Systematic Review with Meta-Analysis and Meta-regression.

Obesity surgery·2025
Same author

Apolipoproteins in Chronic Kidney Disease and Kidney Transplant: A Long Unfinished Story.

International journal of molecular sciences·2025
Same author

Predictors of cognitive performance in idiopathic adult-onset dystonia.

Journal of neural transmission (Vienna, Austria : 1996)·2025
Same author

"Voclosporin in late onset lupus nephritis with anti-PLA2R antibodies".

Seminars in arthritis and rheumatism·2025

NR2B subunit antagonists block post-stroke long-term potentiation (LTP) and reduce brain damage, while preserving normal LTP in stroke models. This suggests NR2B plays a key role in ischemic brain injury.

Area of Science:

  • Neuroscience
  • Neuropharmacology
  • Stroke Research

Background:

  • N-methyl-D-aspartate (NMDA) receptors, particularly those containing the NR2B subunit, are implicated in neuronal function and injury.
  • Activity-dependent long-term potentiation (LTP) is a key mechanism for learning and memory.
  • Ischemia-induced LTP (postischemic LTP) and neuronal damage are significant consequences of stroke.

Purpose of the Study:

  • To investigate the specific role of the NR2B subunit in activity-dependent LTP and postischemic LTP.
  • To evaluate the therapeutic potential of NR2B antagonists in reducing neuronal damage and improving outcomes following focal ischemia.

Main Methods:

  • Utilized rat corticostriatal slice preparations for in vitro experiments.
  • Induced in vitro ischemia using oxygen and glucose deprivation.

Related Experiment Videos

  • Performed in vivo focal ischemia via middle cerebral artery occlusion and recorded intracellularly in the ischemic penumbra.

    • Main Results:

    • NR2B subunit antagonists selectively inhibited postischemic LTP but not activity-dependent LTP.
    • In vivo blockade of NR2B subunits reduced brain damage and improved neurological outcomes in a focal ischemia model.
    • NR2B antagonism rescued activity-dependent LTP in the ischemic penumbra.

    Conclusions:

    • NR2B subunits are critical contributors to striatal damage during both in vitro and in vivo ischemia.
    • NR2B plays a pivotal role in the induction of postischemic LTP.
    • Targeting NR2B subunits may offer a therapeutic strategy for stroke by mitigating ischemic damage and restoring synaptic plasticity.