WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience
QUICK SEARCH:   [advanced]


     
-


HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP
The Journal of Neuroscience, September 16, 2009, 29(37):11441-11450; doi:10.1523/JNEUROSCI.2387-09.2009

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Data
Right arrow Submit an eLetter
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Google Scholar
Right arrow Articles by Christie, J. M.
Right arrow Articles by Jahr, C. E.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Christie, J. M.
Right arrow Articles by Jahr, C. E.

 Previous Article  |  Next Article 

Cellular/Molecular
Selective Expression of Ligand-Gated Ion Channels in L5 Pyramidal Cell Axons

Jason M. Christie and Craig E. Jahr

Vollum Institute, Oregon Health & Science University, Portland, Oregon 97239

Correspondence should be addressed to Dr. Jason M. Christie, Vollum Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239. Email: christij{at}ohsu.edu

NMDA receptor (NMDAR)-dependent strengthening of neurotransmitter release has been widely observed, including in layer 5 (L5) pyramidal cells of the visual cortex, and is attributed to the axonal expression of NMDARs. However, we failed to detect NMDAR-mediated depolarizations or Ca2+ entry in L5 pyramidal cell axons when focally stimulated with NMDAR agonists. This suggests that NMDARs are excluded from the axon. In contrast, local GABAA receptor activation alters axonal excitability, indicating that exclusion of ligand-gated ion channels from the axon is not absolute. Because NMDARs are restricted to the dendrite, NMDARs must signal to the axon by an indirect mechanism to alter release. Although subthreshold somatic depolarizations were found to spread electrotonically hundreds of micrometers through the axon, the resulting axonal potential was insufficient to open voltage-sensitive Ca2+ channels. Therefore, if NMDAR-mediated facilitation of release is cell autonomous, it may depend on voltage signaling but apparently is independent of changes in basal Ca2+. Alternatively, this facilitation may be even less direct, requiring a cascade of events that are merely triggered by NMDAR activation.

Received May 20, 2009; revised June 23, 2009; accepted Aug. 2, 2009.

Correspondence should be addressed to Dr. Jason M. Christie, Vollum Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239. Email: christij{at}ohsu.edu






 -
-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help
-
Copyright 2009 by Society for Neuroscience ONLINE ISSN: 1529-2401
-