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The C57BL/6J mouse exhibits sporadic congenital portosystemic shunts

Cudalbu, Cristina ; McLin, Valérie A ; Lei, Hongxia ; Duarte, Joao M N LU orcid ; Rougemont, Anne-Laure ; Oldani, Graziano ; Terraz, Sylvain ; Toso, Christian and Gruetter, Rolf (2013) In PLoS ONE 8(7). p.69782-69782
Abstract

C57BL/6 mice are the most widely used strain of laboratory mice. Using in vivo proton Magnetic Resonance Spectroscopy ((1)H MRS), we have repeatedly observed an abnormal neurochemical profile in the brains of both wild-type and genetically modified mice derived from the C57BL/6J strain, consisting of a several fold increase in cerebral glutamine and two fold decrease in myo-inositol. This strikingly abnormal neurochemical "phenotype" resembles that observed in chronic liver disease or portosystemic shunting and appeared to be independent of transgene, origin or chow and was not associated with liver failure. As many as 25% of animals displayed the abnormal neurochemical profile, questioning the reliability of this model for... (More)

C57BL/6 mice are the most widely used strain of laboratory mice. Using in vivo proton Magnetic Resonance Spectroscopy ((1)H MRS), we have repeatedly observed an abnormal neurochemical profile in the brains of both wild-type and genetically modified mice derived from the C57BL/6J strain, consisting of a several fold increase in cerebral glutamine and two fold decrease in myo-inositol. This strikingly abnormal neurochemical "phenotype" resembles that observed in chronic liver disease or portosystemic shunting and appeared to be independent of transgene, origin or chow and was not associated with liver failure. As many as 25% of animals displayed the abnormal neurochemical profile, questioning the reliability of this model for neurobiology. We conducted an independent study to determine if this neurochemical profile was associated with portosystemic shunting. Our results showed that 100% of the mice with high brain glutamine displayed portosystemic shunting by concomitant portal angiography while all mice with normal brain glutamine did not. Since portosystemic shunting is known to cause alterations in gene expression in many organs including the brain, we conclude that portosystemic shunting may be the most significant problem associated with C57BL/6J inbreeding both for its effect on the central nervous system and for its systemic repercussions.

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author
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publishing date
type
Contribution to journal
publication status
published
keywords
Angiography, Animals, Brain, Glutamine, Immunohistochemistry, Magnetic Resonance Spectroscopy, Mice, Mice, Inbred C57BL, Portasystemic Shunt, Surgical, Journal Article, Research Support, Non-U.S. Gov't
in
PLoS ONE
volume
8
issue
7
pages
69782 - 69782
publisher
Public Library of Science (PLoS)
external identifiers
  • scopus:84880754871
  • pmid:23936100
ISSN
1932-6203
DOI
10.1371/journal.pone.0069782
language
English
LU publication?
no
id
aaa38572-460d-4dce-8a8f-3a2830cf728e
date added to LUP
2017-10-19 15:15:59
date last changed
2024-03-31 17:23:17
@article{aaa38572-460d-4dce-8a8f-3a2830cf728e,
  abstract     = {{<p>C57BL/6 mice are the most widely used strain of laboratory mice. Using in vivo proton Magnetic Resonance Spectroscopy ((1)H MRS), we have repeatedly observed an abnormal neurochemical profile in the brains of both wild-type and genetically modified mice derived from the C57BL/6J strain, consisting of a several fold increase in cerebral glutamine and two fold decrease in myo-inositol. This strikingly abnormal neurochemical "phenotype" resembles that observed in chronic liver disease or portosystemic shunting and appeared to be independent of transgene, origin or chow and was not associated with liver failure. As many as 25% of animals displayed the abnormal neurochemical profile, questioning the reliability of this model for neurobiology. We conducted an independent study to determine if this neurochemical profile was associated with portosystemic shunting. Our results showed that 100% of the mice with high brain glutamine displayed portosystemic shunting by concomitant portal angiography while all mice with normal brain glutamine did not. Since portosystemic shunting is known to cause alterations in gene expression in many organs including the brain, we conclude that portosystemic shunting may be the most significant problem associated with C57BL/6J inbreeding both for its effect on the central nervous system and for its systemic repercussions.</p>}},
  author       = {{Cudalbu, Cristina and McLin, Valérie A and Lei, Hongxia and Duarte, Joao M N and Rougemont, Anne-Laure and Oldani, Graziano and Terraz, Sylvain and Toso, Christian and Gruetter, Rolf}},
  issn         = {{1932-6203}},
  keywords     = {{Angiography; Animals; Brain; Glutamine; Immunohistochemistry; Magnetic Resonance Spectroscopy; Mice; Mice, Inbred C57BL; Portasystemic Shunt, Surgical; Journal Article; Research Support, Non-U.S. Gov't}},
  language     = {{eng}},
  number       = {{7}},
  pages        = {{69782--69782}},
  publisher    = {{Public Library of Science (PLoS)}},
  series       = {{PLoS ONE}},
  title        = {{The C57BL/6J mouse exhibits sporadic congenital portosystemic shunts}},
  url          = {{http://dx.doi.org/10.1371/journal.pone.0069782}},
  doi          = {{10.1371/journal.pone.0069782}},
  volume       = {{8}},
  year         = {{2013}},
}