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 Richerson, G. B.
Right arrow Articles by Gaspary, H. L.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Richerson, G. B.
Right arrow Articles by Gaspary, H. L.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Other

Carrier-mediated GABA Release: Is There a Functional Role?

George B. Richerson

Heidi L. Gaspary

Neurotransmitters are normally released from neurons via calcium-dependent exocytosis of synaptic vesicles. However, after blockade of vesicular release by removal of calcium, or treatment with tetanus toxin, neurotransmitter release can still occur. In the case of GABA, nonvesicular release results from reversal of its uptake transporter, found on both neurons and glia. These GABA transporters are sodium-dependent and electrogenic, and therefore can be induced to operate in reverse by cell depolarization or by breakdown of the sodium gradient. Although demonstrated biochemically, less is known about whether this form of release occurs in vivo or whether it results in electrophysiological effects. Because conditions that favor reversal of the GABA transporter occur during high-frequency firing, nonvesicular GABA release may occur with excessive neuronal activity, such as during seizures. NEUROSCIENTIST 3:151-157, 1997

Key Words: KEY WORDS Seizures • Epilepsy • Synapse • Anticonvulsants • Antiepilepsy drugs

The Neuroscientist, Vol. 3, No. 3, 151-157 (1997)
DOI: 10.1177/107385849700300307
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:


Home page
 J. Neurophysiol.Home page
H. L. Gaspary, W. Wang, and G. B. Richerson
Carrier-Mediated GABA Release Activates GABA Receptors on Hippocampal Neurons
J Neurophysiol, July 1, 1998; 80(1): 270 - 281.
[Abstract] [Full Text] [PDF]


Advertisement