The Neuroscientist

 

Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Click here to sign up for SAGE Journal Email Alerts today!

Sign In to gain access to subscriptions and/or personal tools.
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
Google Scholar
Right arrow Articles by Finkbeiner, S.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Finkbeiner, S.
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?
The Neuroscientist, Vol. 2, No. 3, 139-142 (1996)
DOI: 10.1177/107385849600200307


Other

Neurotrophins and the Synapse

Steven Finkbeiner

Neurotrophins have become the subject of intensive research because they regulate neuronal differentiation and survival during development and may prove to be useful in the treatment of certain neurodegenerative diseases. Neurotrophins regulate neuronal survival through a signaling cascade that depends on gene expression and new protein synthesis. Recently, several laboratories have shown independently that neurotrophins produce rapid and lasting changes in synaptic efficacy in the adult nervous system. Application of certain neurotrophins rapidly potentiates the efficacy of synaptic transmission. Conversely, brain slices from animals deficient for the brain-derived neurotrophic factor gene show marked impairments in long-term potentiation. In vivo application of specific neurotrophins blocks ocular dominance column formation, and ocular dominance depends on activity-dependent synaptogenesis. The mechanisms of neurotrophin-mediated synaptic plasticity are unknown but may involve the same signaling molecules that mediate neurotrophin-induced gene expression. Neurotrophins may prove to be a new class of molecules that regulate synaptic plasticity in the developing and adult nervous system. NEUROSCIENTIST 2:139-142, 1996

Key Words: KEY WORDS Activity-dependent plasticity • BDNF • Ras • NMDA receptor • LTP • hippocampus


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
A. L. Boxer, H. Moreno, B. Rudy, and E. B. Ziff
FGF-2 Potentiates Ca2+-Dependent Inactivation of NMDA Receptor Currents in Hippocampal Neurons
J Neurophysiol, December 1, 1999; 82(6): 3367 - 3377.
[Abstract] [Full Text] [PDF]