PMID- 22434072
OWN - NLM
STAT- MEDLINE
DCOM- 20121015
LR  - 20211203
IS  - 1559-7016 (Electronic)
IS  - 0271-678X (Print)
IS  - 0271-678X (Linking)
VI  - 32
IP  - 8
DP  - 2012 Aug
TI  - Prolonged therapeutic hypothermia does not adversely impact neuroplasticity after 
      global ischemia in rats.
PG  - 1525-34
LID - 10.1038/jcbfm.2012.38 [doi]
AB  - Hypothermia improves clinical outcome after cardiac arrest in adults. Animal data 
      show that a day or more of cooling optimally reduces edema and tissue injury 
      after cerebral ischemia, especially after longer intervention delays. Lengthy 
      treatments, however, may inhibit repair processes (e.g., synaptogenesis). Thus, 
      we evaluated whether unilateral brain hypothermia ( approximately 33 degrees C) affects neuroplasticity 
      in the rat 2-vessel occlusion model. In the first experiment, we cooled starting 
      1 hour after ischemia for 2, 4, or 7 days. Another group was cooled for 2 days 
      starting 48 hours after ischemia. One group remained normothermic throughout. All 
      hypothermia treatments started 1 hour after ischemia equally reduced hippocampal 
      CA1 injury in the cooled hemisphere compared with the normothermic side and the 
      normothermic group. Cooling only on days 3 and 4 was not beneficial. Importantly, 
      no treatment influenced neurogenesis (Ki67/Doublecortin (DCX) staining), synapse 
      formation (synaptophysin), or brain-derived neurotropic factor (BDNF) 
      immunohistochemistry. A second experiment confirmed that BDNF levels (ELISA) were 
      equivalent in normothermic and 7-day cooled rats. Last, we measured zinc (Zn), 
      which is important in plasticity, with X-ray fluorescence imaging in normothermic 
      and 7-day cooled rats. Hypothermia did not alter the postischemic distribution of 
      Zn within the hippocampus. In summary, cooling significantly mitigates injury 
      without compromising neuroplasticity.
FAU - Silasi, Gergely
AU  - Silasi G
AD  - Centre for Neuroscience, University of Alberta, Edmonton, Alberta, Canada.
FAU - Klahr, Ana C
AU  - Klahr AC
FAU - Hackett, Mark J
AU  - Hackett MJ
FAU - Auriat, Angela M
AU  - Auriat AM
FAU - Nichol, Helen
AU  - Nichol H
FAU - Colbourne, Frederick
AU  - Colbourne F
LA  - eng
GR  - P41 RR001209/RR/NCRR NIH HHS/United States
GR  - P41RR001209/RR/NCRR NIH HHS/United States
GR  - CIF 99472/CAPMC/CIHR/Canada
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20120321
PL  - United States
TA  - J Cereb Blood Flow Metab
JT  - Journal of cerebral blood flow and metabolism : official journal of the 
      International Society of Cerebral Blood Flow and Metabolism
JID - 8112566
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Dcx protein, rat)
RN  - 0 (Doublecortin Protein)
RN  - 0 (Synaptophysin)
RN  - J41CSQ7QDS (Zinc)
SB  - IM
MH  - Animals
MH  - Brain Ischemia/metabolism/pathology/physiopathology/*therapy
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - CA1 Region, Hippocampal/metabolism/pathology
MH  - Dentate Gyrus/metabolism/pathology
MH  - Disease Models, Animal
MH  - Doublecortin Protein
MH  - Early Medical Intervention
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Equipment Design
MH  - *Hypothermia, Induced/adverse effects/methods
MH  - Male
MH  - Microglia/metabolism/pathology
MH  - Neuronal Plasticity/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Synaptophysin/metabolism
MH  - Time Factors
MH  - Zinc/metabolism
PMC - PMC3421089
EDAT- 2012/03/22 06:00
MHDA- 2012/10/16 06:00
PMCR- 2013/08/01
CRDT- 2012/03/22 06:00
PHST- 2012/03/22 06:00 [entrez]
PHST- 2012/03/22 06:00 [pubmed]
PHST- 2012/10/16 06:00 [medline]
PHST- 2013/08/01 00:00 [pmc-release]
AID - jcbfm201238 [pii]
AID - 10.1038/jcbfm.2012.38 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 2012 Aug;32(8):1525-34. doi: 10.1038/jcbfm.2012.38. 
      Epub 2012 Mar 21.