SAGE Journals Online
Advertisement
Sign In to gain access to subscriptions and/or personal tools.

 

Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Advertisement

Sign In to gain access to subscriptions and/or personal tools.
The Neuroscientist
This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Mcintosh, T. K.
Right arrow Articles by Raghupathi, R.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Mcintosh, T. K.
Right arrow Articles by Raghupathi, R.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Reviews

REVIEW {blacksquare} : Calcium and the Pathogenesis of Traumatic CNS Injury: Cellular and Molecular Mechanisms

Tracy K. Mcintosh

Head Injury Center Department of Neurosurgery University of Pennsylvania Philadelphia, Pennsylvania

Kathryn E. Saatman

Head Injury Center Department of Neurosurgery University of Pennsylvania Philadelphia, Pennsylvania

Ramesh Raghupathi

Head Injury Center Department of Neurosurgery University of Pennsylvania Philadelphia, Pennsylvania

Under normal conditions in the central nervous system (CNS), the calcium ion (Ca2+) is known to mediate a variety of neuronal functions, including synaptic neurotransmitter release, neuronal plasticity, protein phos phorylation, and gene expression. Whereas intracellular calcium concentrations ([Ca2+]i) are precisely reg ulated through intracellular buffering, binding, and sequestration, alterations in calcium ion homeostasis and influx of Ca 2+ have been implicated in the pathogenesis of neuronal death and degeneration, as well as cerebral vasospasm associated with multiple types of CNS injury. This review revisits the "calcium hypoth esis" of neuronal death associated with traumatic injury to the CNS and examines both the direct and indirect molecular and cellular evidence for calcium-mediated neuropathology, as well as the potential for novel therapeutic strategies targeted at the downstream intracellular effects of calcium signaling and calcium- activated neutral protease (calpain) activation. NEUROSCIENTIST 3:169-175, 1997

Key Words: KEY WORDS Brain injury • Calcium • Calpain • Cell death • Gene expression

The Neuroscientist, Vol. 3, No. 3, 169-175 (1997)
DOI: 10.1177/107385849700300310
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 J. Neurophysiol.Home page
D. Murchison and W. H. Griffith
Increased Calcium Buffering in Basal Forebrain Neurons During Aging
J Neurophysiol, July 1, 1998; 80(1): 350 - 364.
[Abstract] [Full Text] [PDF]


Advertisement