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

Protein kinase C and synaptic dysfunction after cardiac arrest.

Miguel A Perez-Pinzon1, Ami P Raval, Kunjan R Dave

  • 1Cerebral Vascular Disease Research Center, Department of Neurology (D4-5) and Neuroscience Program, University of Miami School of Medicine, PO Box 016960, Miami, FL-33101, USA.

Pathophysiology : the Official Journal of the International Society for Pathophysiology
|June 2, 2005
PubMed
Summary

Neuronal cell death after cardiac arrest (CA) involves complex mechanisms, including delayed neuronal death and synaptic dysfunction. Protein kinase C (PKC) may play a role in these CA-induced synaptic problems.

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

Electronic cigarette vapor exposure modifies stroke-induced transcriptional and microglial responses in a sex-dependent manner.

Neurochemistry international·2026
Same author

The cognitive consequences of hypoglycemia in diabetes.

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·2026
Same author

Thomas Willis Lecture Award: Nature's Blueprint for Ischemic Tolerance: Preconditioning and Postconditioning Strategies.

Stroke·2026
Same author

From menarche to menopause: estrogenic influences on stroke-related depression in women.

Frontiers in neuroendocrinology·2026
Same author

Preservation of Septo-Hippocampal Theta Oscillations via Cholinergic Protection Underlies Cognitive Recovery After Physical Exercise Post-Cardiac Arrest.

Stroke·2025
Same author

Enhanced risk of thrombosis in aged insulin-treated diabetic rats exposed to non-severe recurrent hypoglycemia.

Diabetology & metabolic syndrome·2025

Area of Science:

  • Neuroscience
  • Cardiovascular Research
  • Cellular Biology

Background:

  • Neuronal cell death following cardiac arrest (CA) is a complex, multi-stage process.
  • Delayed neuronal death occurs over days to months post-ischemia, impacting long-term survivors.
  • Synaptic dysfunction is a significant consequence of CA, contributing to cognitive deficits.

Purpose of the Study:

  • To review synaptic dysfunction mechanisms after CA.
  • To explore the potential role of Protein Kinase C (PKC) in post-CA synaptic derangements.

Main Methods:

  • Literature review of studies on cardiac arrest, neuronal death, and synaptic plasticity.
  • Analysis of research implicating PKC in neuronal function and cell death pathways.

Related Experiment Videos

Main Results:

  • Electrophysiological changes precede morphological deterioration in post-CA neurons.
  • Impaired cognitive functions, such as memory deficits, are common in CA survivors.
  • PKC is a key regulator of synaptic function and implicated in cerebral ischemia-induced cell death.

Conclusions:

  • Synaptic dysfunction is a critical component of neuronal damage after CA.
  • PKC emerges as a potential key modulator of synaptic dysfunction and delayed neuronal death following CA.