J Physiol Wellcome Trust-funded researchers
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Physiology in Press

First published online on March 8, 2007.
 Copyright © 2007 by The Physiological Society
This Article
Right arrow Full Text (Rapid PDF)
Right arrow Supplemental data
Right arrow All Versions of this Article:
581/2/619    most recent
jphysiol.2007.127860v1
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Schmidt, H.
Right arrow Articles by Eilers, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schmidt, H.
Right arrow Articles by Eilers, J.

Received January 9, 2007
Revised February 5, 2007
Accepted after revision March 6, 2007

Spino-dendritic crosstalk in rodent Purkinje neurons mediated by endogenous Ca2+-binding proteins

Hartmut Schmidt1*, Svenja Kunerth2, Christian Wilms1, Rainer Strotmann3, and Jens Eilers1

1 Carl-Ludwig-Institute for Physiology
2 Olympus Germany
3 Institute for Biochemistry

* To whom correspondence should be addressed. E-mail: hartmut.schmidt{at}medizin.uni-leipzig.de.

The range of action of the second messenger Ca2+ is a key determinant of neuronal excitability and plasticity. For dendritic spines, there is ongoing debate about in as much diffusional efflux of Ca2+ affects spine signalling. However, the consequences of spino-dendritic coupling for the dendritic Ca2+ homeostasis and downstream signalling cascades have not been explored to date. We addressed this question by 4D computer simulations, which were based on Ca2+-imaging data from mice that either express or lack distinct endogenous Ca2+-binding proteins. Our simulations revealed that single active spines do not affect dendritic Ca2+ signalling. Neighbouring, coactive spines, however, induce sizable increases in dendritic [Ca2+]i when they process slow synaptic Ca2+ signals, as those implicated in the induction of long-term plasticity. This spino-dendritic coupling is mediated by buffered diffusion, specifically by diffusing calbindin-bound Ca2+. It represents a central mechanism for activating calmodulin in dendritic shafts and, therefore, a novel form of signal integration in spiny dendrites.


Key words: Calcium (Ca2+) • Calcium (Ca2+) buffer • Diffusion




This article has been cited by other articles:


Home page
 Physiol. Rev.Home page
P. J. Sjostrom, E. A. Rancz, A. Roth, and M. Hausser
Dendritic Excitability and Synaptic Plasticity
Physiol Rev, April 1, 2008; 88(2): 769 - 840.
[Abstract] [Full Text] [PDF]

Home page
 Biophys. JHome page
L. A. Mironova and S. L. Mironov
Approximate Analytical Time-Dependent Solutions to Describe Large-Amplitude Local Calcium Transients in the Presence of Buffers
Biophys. J., January 15, 2008; 94(2): 349 - 358.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
A. Nemri and N. Ghisovan
Dendritic spines: it takes two to make an impression
J. Physiol., July 1, 2007; 582(1): 15 - 16.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2007 The Physiological Society.