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Actin redistribution underlies the sparing effect of mild hypothermia on dendritic spine morphology after in vitro ischemia.

Gisselsson, Lennart LU ; Matus, Andrew and Wieloch, Tadeusz LU (2005) In Journal of Cerebral Blood Flow and Metabolism 25(10). p.1346-1355
Abstract
Brain hypothermia is at present the most effective neuroprotective treatment against brain ischemia in man. Ischemia induces a redistribution of proteins involved in synaptic functions, which is markedly diminished by therapeutic hypothermia (33 degrees C). Dendritic spines at excitatory synapses are motile and show both shape changes and rearrangement of synaptic proteins as a consequence of neuronal activity. We investigated the effect of reduced temperature (33 degrees C and 27 degrees C compared with 37 degrees C), on spine motility, length and morphology by studying the distribution of GFP-actin before, during and after induction of in vitro ischemia. Because high-concentration actin filaments are located inside spines, dissociated... (More)
Brain hypothermia is at present the most effective neuroprotective treatment against brain ischemia in man. Ischemia induces a redistribution of proteins involved in synaptic functions, which is markedly diminished by therapeutic hypothermia (33 degrees C). Dendritic spines at excitatory synapses are motile and show both shape changes and rearrangement of synaptic proteins as a consequence of neuronal activity. We investigated the effect of reduced temperature (33 degrees C and 27 degrees C compared with 37 degrees C), on spine motility, length and morphology by studying the distribution of GFP-actin before, during and after induction of in vitro ischemia. Because high-concentration actin filaments are located inside spines, dissociated hippocampal neurons (7-11 DIV) from transgenic mice expressing GFP-actin were used in this study. The movement of the spines and the distribution of GFP-actin were recorded using time-lapse fluorescence microscopy. Under normal conditions rapid rearrangement of GFP-actin was seen in dendritic spines, indicating highly motile spines at 37 degrees C. Decreasing the incubation temperature to 33 degrees C or 27 degrees C, dramatically reduces actin dynamics (spine motility) by approximately 50% and 70%, respectively. In addition, the length of the spine shaft was reduced by 20%. We propose that decreasing the temperature from 37 degrees C to 33 degrees C during ischemia decreases the neuronal actin polymerization rate, which reduces spine calcium kinetics, disrupts detrimental cell signaling and protects neurons against damage. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
motility, cytoskeleton, dendritic spines, neurotransmission, OGD, GFP-actin
in
Journal of Cerebral Blood Flow and Metabolism
volume
25
issue
10
pages
1346 - 1355
publisher
Nature Publishing Group
external identifiers
  • pmid:15874974
  • wos:000232253800010
  • scopus:25144455054
ISSN
1559-7016
DOI
10.1038/sj.jcbfm.9600131
language
English
LU publication?
yes
id
cb99b570-58c8-4a6d-becc-67642b115c04 (old id 138185)
alternative location
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=15874974&dopt=Abstract
date added to LUP
2007-07-13 14:17:01
date last changed
2017-08-27 05:09:37
@article{cb99b570-58c8-4a6d-becc-67642b115c04,
  abstract     = {Brain hypothermia is at present the most effective neuroprotective treatment against brain ischemia in man. Ischemia induces a redistribution of proteins involved in synaptic functions, which is markedly diminished by therapeutic hypothermia (33 degrees C). Dendritic spines at excitatory synapses are motile and show both shape changes and rearrangement of synaptic proteins as a consequence of neuronal activity. We investigated the effect of reduced temperature (33 degrees C and 27 degrees C compared with 37 degrees C), on spine motility, length and morphology by studying the distribution of GFP-actin before, during and after induction of in vitro ischemia. Because high-concentration actin filaments are located inside spines, dissociated hippocampal neurons (7-11 DIV) from transgenic mice expressing GFP-actin were used in this study. The movement of the spines and the distribution of GFP-actin were recorded using time-lapse fluorescence microscopy. Under normal conditions rapid rearrangement of GFP-actin was seen in dendritic spines, indicating highly motile spines at 37 degrees C. Decreasing the incubation temperature to 33 degrees C or 27 degrees C, dramatically reduces actin dynamics (spine motility) by approximately 50% and 70%, respectively. In addition, the length of the spine shaft was reduced by 20%. We propose that decreasing the temperature from 37 degrees C to 33 degrees C during ischemia decreases the neuronal actin polymerization rate, which reduces spine calcium kinetics, disrupts detrimental cell signaling and protects neurons against damage.},
  author       = {Gisselsson, Lennart and Matus, Andrew and Wieloch, Tadeusz},
  issn         = {1559-7016},
  keyword      = {motility,cytoskeleton,dendritic spines,neurotransmission,OGD,GFP-actin},
  language     = {eng},
  number       = {10},
  pages        = {1346--1355},
  publisher    = {Nature Publishing Group},
  series       = {Journal of Cerebral Blood Flow and Metabolism},
  title        = {Actin redistribution underlies the sparing effect of mild hypothermia on dendritic spine morphology after in vitro ischemia.},
  url          = {http://dx.doi.org/10.1038/sj.jcbfm.9600131},
  volume       = {25},
  year         = {2005},
}