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

New CNS-specific calcium antagonists.

R N McBurney1, D Daly, J B Fischer

  • 1Cambridge NeuroScience, Inc., Massachusetts.

Journal of Neurotrauma
|May 1, 1992
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

Taking the 'HIT' (Heparin-induced thrombocytopenia) - Balancing Local Testing with Delayed Central Results.

Irish medical journal·2026
Same author

Impact of a trauma bypass protocol on a receiving Emergency Department: a 4-year review.

Irish medical journal·2025
Same author

Influence of study design on effects of mask wearing on fMRI BOLD contrast and systemic physiology - A comment on Law et al. (2021).

NeuroImage·2021
Same author

Two-layered susceptibility vessel sign is associated with biochemically quantified thrombus red blood cell content.

European journal of neurology·2020
Same author

Health economic analysis of a cluster-randomised trial (OptiBIRTH) designed to increase rates of vaginal birth after caesarean section.

BJOG : an international journal of obstetrics and gynaecology·2019
Same author

Persistent effects of pre-Columbian plant domestication on Amazonian forest composition.

Science (New York, N.Y.)·2017
Same journal

Urinary Tract Infection Exaggerates Cognitive Deficits and Region-Specific Neuroinflammation Following Traumatic Brain Injury.

Journal of neurotrauma·2026
Same journal

Fall Risk and Physical/Occupational Therapy Referral Patterns in Older Adults with Mild Traumatic Brain Injury.

Journal of neurotrauma·2026
Same journal

The Effects of High-Thoracic Spinal Cord Injury on the Heart Transcriptome.

Journal of neurotrauma·2026
Same journal

Rigor and Transparency in Two Neurotrauma-Publishing Journals: Editorial Policies Improve Transparent Reporting.

Journal of neurotrauma·2026
Same journal

Neuroimaging and Fluid-Based Biomarkers in Sport-Related Concussion in Female Athletes: A Scoping Review.

Journal of neurotrauma·2026
Same journal

Transcranial Photobiomodulation Promotes Neurological Resilience in Current Collegiate American Football Players Exposed to Repetitive Head Acceleration Events.

Journal of neurotrauma·2026
See all related articles

New compounds, CNS 2103 and CNS 1145, show promise in treating ischemic brain injury by blocking excessive calcium entry and glutamate release, key factors in stroke and traumatic brain injury cell death.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Ischemic brain injuries, such as stroke and traumatic brain injury, cause excessive glutamate release.
  • This glutamate stimulates massive calcium influx into neurons, triggering cell death pathways.
  • High-threshold calcium channels, particularly R-type channels, are major contributors to this calcium entry.

Purpose of the Study:

  • To investigate novel compounds for treating ischemic brain injury.
  • To explore the potential of blocking specific calcium channels and glutamate release.

Main Methods:

  • Development of CNS 2103, a spider venom-derived compound targeting R-type and L-type calcium channels.
  • Development of CNS 1145, a substituted guanidine using a rapid kinetic approach to monitor glutamate release.

Related Experiment Videos

  • Assessing the blockade of calcium-dependent glutamate release mediated by persistent depolarization.

    • Main Results:

    • CNS 2103 antagonizes both R-type and L-type calcium channels, showing selectivity for calcium channels.
    • CNS 1145 selectively blocks a component of calcium-dependent glutamate release.
    • Evidence suggests CNS 1145 antagonizes presynaptic N-type calcium channels, reducing glutamate release.

    Conclusions:

    • CNS 2103 is a promising lead compound for ischemic brain injury due to its broad calcium channel antagonism.
    • CNS 1145 effectively blocks glutamate release, potentially by antagonizing N-type calcium channels.
    • These compounds offer potential therapeutic strategies for mitigating neuronal damage in ischemic conditions.