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

Seizures, brain damage and brain development

C G Wasterlain1, Y Shirasaka

  • 1Epilepsy Research, Veterans Affairs Medical Center, Sepulveda, CA.

Brain & Development
|July 1, 1994
PubMed
Summary
This summary is machine-generated.

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

Interindividual variability of CYP2C19-catalyzed drug metabolism due to differences in gene diplotypes and cytochrome P450 oxidoreductase content.

The pharmacogenomics journal·2015
Same author

Hyperthermia aggravates status epilepticus-induced epileptogenesis and neuronal loss in immature rats.

Neuroscience·2015
Same author

Advances in the pathophysiology of status epilepticus.

Acta neurologica Scandinavica. Supplementum·2007
Same author

Advances in the pathophysiology of status epilepticus.

Acta neurologica Scandinavica·2007
Same author

Mitochondrial pathways of neuronal necrosis.

Biochemical Society transactions·2006
Same author

Hypoxia in presence of blockers of excitotoxicity induces a caspase-dependent neuronal necrosis.

Neuroscience·2006
Same journal

Association of relative age with medical consultations for developmental concerns: A nationwide birth cohort study in Japan.

Brain & development·2026
Same journal

Extending the combined N-back/Nogo paradigm: Toward subtype-sensitive and translationally meaningful ERP research in ADHD.

Brain & development·2026
Same journal

Receptor-specific dopaminergic imbalance and sensory gating in Lesch-Nyhan syndrome.

Brain & development·2026
Same journal

From weather stations to the home environment: Refining seizure prediction in pediatric drug-resistant epilepsy.

Brain & development·2026
Same journal

Pediatric GBS-myelitis overlap syndrome: Severe phenotype, treatment response, and neurological outcomes.

Brain & development·2026
Same journal

Aspartoacylase (ASPA) gene mutations and neuroimaging features in Iranian patients with Canavan disease: a descriptive study.

Brain & development·2026
See all related articles

Seizures can damage the hippocampus, leading to chronic epilepsy through excitotoxicity and altered neural circuits. Understanding these mechanisms, especially in the developing brain, is crucial for future epilepsy treatments.

Area of Science:

  • Neuroscience
  • Epileptology
  • Developmental Neuroscience

Background:

  • Hippocampal damage is linked to both seizure activity and the development of chronic epilepsy.
  • Excitotoxic mechanisms, primarily involving N-methyl-D-aspartate (NMDA) receptors, are implicated in status epilepticus-induced brain damage.

Purpose of the Study:

  • To review current models of status epilepticus-induced brain damage.
  • To explore the mechanisms by which seizure-induced hippocampal lesions cause chronic epilepsy.
  • To investigate the unique vulnerabilities of the immature brain to seizure activity.

Main Methods:

  • Review of current animal models of status epilepticus.
  • Analysis of excitotoxic mechanisms and glutamate receptor involvement (NMDA and non-NMDA).

Related Experiment Videos

  • Examination of developmental differences in brain vulnerability to seizures.

    • Main Results:

    • Excitotoxicity, mediated by NMDA and non-NMDA receptors, is a key mechanism in seizure-induced brain damage.
    • The immature brain exhibits distinct vulnerabilities and resistance patterns compared to the adult brain.
    • Hippocampal circuit rearrangement, involving interneuron loss or excitatory neuron misdirection, contributes to chronic epilepsy.

    Conclusions:

    • Seizure-induced hippocampal lesions can lead to chronic epilepsy via altered inhibition, aberrant excitatory connections, or facilitated kindling.
    • Findings reconcile experimental animal models with human hippocampal pathology in intractable epilepsy.
    • Interneurons in the dentate gyrus play a critical role in epileptogenesis, supporting the concept that 'seizures beget seizures'.