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

Cellular alterations associated with perinatal asphyxia

M V Johnston1

  • 1Department of Neurology, Johns Hopkins University, School of Medicine, Baltimore, Maryland.

Clinical and Investigative Medicine. Medecine Clinique Et Experimentale
|April 1, 1993
PubMed
Summary

Asphyxia causes cell damage through biochemical changes like ion imbalance and neurotransmitter release, leading to cell death. Research aims to understand these mechanisms to protect brain tissue.

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

Sleep dysfunction following neonatal ischemic seizures are differential by neonatal age of insult as determined by qEEG in a mouse model.

Neurobiology of disease·2018
Same author

Apparent proton affinities of highly charged peptide ions.

Journal of the American Society for Mass Spectrometry·2016
Same author

Excitotoxicity as a Common Mechanism for Fetal Neuronal Injury with Hypoxia and Intrauterine Inflammation.

Advances in pharmacology (San Diego, Calif.)·2016
Same author

Cerebral Reorganization after Hemispherectomy: A DTI Study.

AJNR. American journal of neuroradiology·2016
Same author

Transfontanellar duplex brain ultrasonography resistive indices as a prognostic tool in neonatal hypoxic-ischemic encephalopathy before and after treatment with therapeutic hypothermia.

Journal of perinatology : official journal of the California Perinatal Association·2015
Same author

Acute TrkB inhibition rescues phenobarbital-resistant seizures in a mouse model of neonatal ischemia.

The European journal of neuroscience·2015

Area of Science:

  • Biochemistry
  • Neuroscience
  • Cellular Biology

Background:

  • Asphyxia induces cellular biochemical events, altering function and potentially causing cell death.
  • Tissue hypoxia and ischemia disrupt neuronal membranes, ion balance, and energy metabolism.
  • Neurotransmitter imbalances, particularly glutamate excitotoxicity, are key features.

Purpose of the Study:

  • To elucidate the biochemical cascade initiated by asphyxia.
  • To understand the mechanisms of neuronal cell death following asphyxia.
  • To identify therapeutic targets for salvaging brain tissue.

Main Methods:

  • Analysis of cellular biochemical events following asphyxia.
  • Investigation of neuronal membrane depolarization and ion homeostasis.
  • Assessment of neurotransmitter dynamics, focusing on glutamate.
  • Examination of intracellular calcium accumulation pathways.
  • Evaluation of downstream effectors like proteases and free radicals.

Main Results:

  • Asphyxia leads to neuronal membrane depolarization and altered ion homeostasis.
  • Enhanced glutamate release and impaired re-uptake contribute to excitotoxicity.
  • Multiple factors drive abnormal intracellular calcium accumulation.
  • Elevated calcium activates destructive cellular pathways, including proteases and free radical generation.
  • These synergistic processes result in cellular necrosis within minutes to hours.

Conclusions:

  • Asphyxia triggers a complex cascade of biochemical events culminating in neuronal cell death.
  • Intracellular calcium overload is a critical mediator of asphyxial brain injury.
  • Understanding these mechanisms is crucial for developing neuroprotective strategies.

Related Experiment Videos