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

Polyamines in cerebral ischemia.

W Paschen1, R Schmidt-Kastner, J Hallmayer

  • 1Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Cologne, Merheim, FRG.

Neurochemical Pathology
|July 1, 1988
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

08-05 'Kraepelinian' and 'Bleulerian' schizophrenia: a genetic dissection of a cognitive endophenotype.

Acta neuropsychiatrica·2016
Same author

Telomere length and cortisol reactivity in children of depressed mothers.

Molecular psychiatry·2014
Same author

Differential distribution of hypoxia-inducible factor 1-beta (ARNT or ARNT2) in mouse substantia nigra and ventral tegmental area.

Journal of chemical neuroanatomy·2014
Same author

Transient ischemia induces massive nuclear accumulation of SUMO2/3-conjugated proteins in spinal cord neurons.

Spinal cord·2012
Same author

An environmental analysis of genes associated with schizophrenia: hypoxia and vascular factors as interacting elements in the neurodevelopmental model.

Molecular psychiatry·2012
Same author

Visualization of axonal degeneration after optic nerve lesion in rat by immunohistochemical labelling for myelin basic protein (MBP).

Restorative neurology and neuroscience·2011
Same journal

Role of circulatory disturbances in the development of post-ischemic brain edema.

Neurochemical pathology·1988
Same journal

Brain ion homeostasis in cerebral ischemia.

Neurochemical pathology·1988
Same journal

Compartmentation of acid-base balance in brain during complete ischemia.

Neurochemical pathology·1988
Same journal

Regional pH and electrolyte homeostasis of cat brain after prolonged ischemia.

Neurochemical pathology·1988
Same journal

Molecular mechanisms of glial swelling in vitro.

Neurochemical pathology·1988
Same journal

Acidosis and ischemic brain damage.

Neurochemical pathology·1988
See all related articles

Polyamines like putrescine increase dramatically after cerebral ischemia and reperfusion. Elevated putrescine levels correlate with ischemic cell damage, suggesting its potential as a biochemical marker for brain injury.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Cerebral ischemia can lead to significant brain damage.
  • Polyamines are crucial for cellular functions and have been implicated in various neurological conditions.

Purpose of the Study:

  • To investigate regional polyamine profiles (putrescine, spermidine, spermine) in reversible cerebral ischemia.
  • To determine the correlation between polyamine changes and ischemic cell injury.

Main Methods:

  • Induction of reversible cerebral ischemia in rats and Mongolian gerbils.
  • Analysis of polyamine levels in brain tissue during ischemia and recirculation.
  • Correlation of polyamine concentrations with histological assessment of cell injury.

Main Results:

Related Experiment Videos

  • Polyamine profiles remained unchanged during ischemia but altered significantly after recirculation.
  • A substantial increase in putrescine and a decrease in spermine were observed in severely damaged brain regions.
  • Postischemic putrescine levels strongly correlated with the extent of ischemic cell injury and ischemia duration.
  • Putrescine elevation was detected in the hippocampus even before visible cell damage became apparent.

Conclusions:

  • Putrescine serves as a reliable biochemical marker for ischemic cell injury.
  • Postischemic polyamine alterations, particularly putrescine increase, reflect the severity of brain damage following ischemia.
  • These findings contribute to understanding the biochemical consequences of ischemic events in the brain.