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Developmental profile of localized spontaneous Ca2+ release events in the dendrites of rat hippocampal pyramidal neurons
Authors
Allbritton
Baylor
+51 more
Baylor
Berlin
Berrout
Borst
Bortolozzi
Cheng
Cheng
Cornelisse
Faas
Felder
Franzini-Armstrong
Goldberg
Gómez
Hagenston
Helmchen
Hertle
Hines
Hodgkin
Holbro
Hollingworth
Jayasinghe
Kay
Kenichi Miyazaki
Kip
Koizumi
Kovacs
Kushmerick
Lacampagne
Lasser-Ross
Llinás
Lohmann
Manita
Manita
Maravall
Nakamura
Nakamura
Neher
Parker
Power
Sabatini
Sala
Satoshi Manita
Shuai
Smith
Spigelman
Stuart
Tsugorka
Verkhratsky
William N. Ross
Yasuda
Zhang
Publication date
1 August 2012
Publisher
'Elsevier BV'
Doi
View
on
PubMed
Abstract
Author Posting. © The Author(s), 2012. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Cell Calcium 52 (2012): 422-432, doi:10.1016/j.ceca.2012.08.001.Recent experiments demonstrate that localized spontaneous Ca2+ release events can be detected in the dendrites of pyramidal cells in the hippocampus and other neurons (J. Neurosci. 29:7833-7845, 2009). These events have some properties that resemble ryanodine receptor mediated “sparks” in myocytes, and some that resemble IP3 receptor mediated “puffs” in oocytes. They can be detected in the dendrites of rats of all tested ages between P3 and P80 (with sparser sampling in older rats), suggesting that they serve a general signaling function and are not just important in development. However, in younger rats the amplitudes of the events are larger than the amplitudes in older animals and almost as large as the amplitudes of Ca2+ signals from backpropagating action potentials (bAPs). The rise time of the event signal is fast at all ages and is comparable to the rise time of the bAP fluorescence signal at the same dendritic location. The decay time is slower in younger animals, primarily because of weaker Ca2+ extrusion mechanisms at that age. Diffusion away from a brief localized source is the major determinant of decay at all ages. A simple computational model closely simulates these events with extrusion rate the only age dependent variable.Supported in part by NIH grant NS-016295
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