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

Ischemia and lesion induced imbalances in cortical function

H J Luhmann1

  • 1Department of Neurophysiology, University of Düsseldorf, Germany. luhmann@uni-duesseldorf.de

Progress in Neurobiology
|February 1, 1996
PubMed
Summary

Early intervention targeting rapid cellular changes is crucial for managing brain lesions from hypoxia or ischemia. Broad-acting drugs may offer better neuroprotection than single-target therapies, especially considering age-dependent responses in developing brains.

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

Probabilistic graphical model identifies clusters of EEG patterns in recordings from neonates.

Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology·2019
Same author

Co-activation of VEGF and NMDA receptors promotes synaptic targeting of AMPA receptors.

Molecular psychiatry·2016
Same author

A critical role for VEGF and VEGFR2 in NMDA receptor synaptic function and fear-related behavior.

Molecular psychiatry·2016
Same author

GABA transporters control GABAergic neurotransmission in the mouse subplate.

Neuroscience·2015
Same author

Methylxanthine-evoked perturbation of spontaneous and evoked activities in isolated newborn rat hippocampal networks.

Neuroscience·2015
Same author

Cajal-Retzius cells: update on structural and functional properties of these mystic neurons that bridged the 20th century.

Neuroscience·2014

Area of Science:

  • Neuroscience
  • Cerebral Ischemia Research
  • Traumatic Brain Injury

Background:

  • Ischemic and traumatic brain lesions severely impact cortical structures, causing functional deficits.
  • Early cellular events include membrane depolarization, suppressed inhibition, and enhanced excitation, leading to hyperexcitability and cell death.
  • Existing treatments like calcium and NMDA antagonists have shown limited clinical success.

Purpose of the Study:

  • To investigate the early cellular mechanisms underlying cortical damage from hypoxia and ischemia.
  • To explore the potential of broad-spectrum pharmacological interventions for neuroprotection.
  • To examine age-dependent differences in cortical responses to ischemic insults.

Main Methods:

  • Analysis of cellular membrane properties and synaptic network interactions following ischemic/hypoxic events.

Related Experiment Videos

  • Review of pharmacological strategies targeting ligand-activated receptors and voltage-dependent channels.
  • Comparative study of adult versus immature cortical responses to brain injury.

    • Main Results:

    • Rapid functional modifications, including membrane depolarization and altered synaptic transmission, occur within minutes of hypoxia/ischemia.
    • These early changes are proposed triggers for neuronal hyperexcitability and subsequent cell death.
    • Immature cortical networks exhibit distinct responses to insults due to higher synaptic plasticity and age-dependent factors.

    Conclusions:

    • Early, powerful interventions targeting multiple cellular pathways are essential to prevent lesion expansion.
    • Broad-spectrum agents acting on various receptors and channels, including vascular effects, may be more effective.
    • Therapeutic strategies for adult ischemic injury may not directly translate to the immature brain, necessitating further research into age-specific treatments.