Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2009-3-30
pubmed:abstractText
Mice with reduced expression of the NR1 subunit of the NMDA receptor (NR1 hypomorphic mice) display altered behavioral phenotypes that may relate to behavioral characteristics of schizophrenia. Altered phenotypes in the NR1 hypomorphs include marked deficits in species-typical behavioral interactions in tests of social aggression and social affiliation. To gain insight into neuroanatomical circuits disrupted by reduced NMDA receptor function, the present work compared regional brain activation in NR1 hypomorphic mice and their wild type controls after a resident-intruder test. Induction of Fos protein was used as an index of neuronal activation. Wild type mice exhibited robust induction of Fos in select brain regions, including specific nuclei of the hypothalamus and amygdala, lateral septum, and widespread regions of the cerebral cortex. Although the behavioral patterns were different for male and female mice, neuroanatomical patterns of Fos induction were remarkably similar for the two sexes. To determine socially specific components of Fos induction by the resident-intruder test, responses were compared for mice assessed in a test of general arousal and stress involving forced swim. Some common brain regions were activated by both tests but regionally specific differences were also found. The NR1 hypomorphic mice tested in the resident-intruder procedure displayed distinctly different behavioral interactions compared to the wild type mice and exhibited a significantly blunted Fos response in almost all brain regions. The mutant mice also exhibited reduced Fos in response to swim stress in specific brain regions. These data suggest that the NR1 hypomorphic mice have functional activation deficits in response to social challenge and swim stress.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-10481908, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-11557159, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-12657691, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-15265649, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-15283961, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-15467708, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-15496680, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-15745956, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-15885690, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-16046005, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-16263109, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-16362405, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-1654746, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-16638606, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-16687160, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-17318306, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-17712349, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-18185498, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-18550035, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-7492260, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-7644033, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-8122957, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-8526975, http://linkedlifedata.com/resource/pubmed/commentcorrection/19232330-9518601
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1872-6240
pubmed:author
pubmed:issnType
Electronic
pubmed:day
10
pubmed:volume
1265
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
186-95
pubmed:dateRevised
2010-9-23
pubmed:meshHeading
pubmed-meshheading:19232330-Aggression, pubmed-meshheading:19232330-Amygdala, pubmed-meshheading:19232330-Animals, pubmed-meshheading:19232330-Cerebral Cortex, pubmed-meshheading:19232330-Female, pubmed-meshheading:19232330-Functional Laterality, pubmed-meshheading:19232330-Hypothalamus, pubmed-meshheading:19232330-Immunohistochemistry, pubmed-meshheading:19232330-Male, pubmed-meshheading:19232330-Mice, pubmed-meshheading:19232330-Mice, Inbred C57BL, pubmed-meshheading:19232330-Mice, Inbred DBA, pubmed-meshheading:19232330-Mice, Transgenic, pubmed-meshheading:19232330-Motor Activity, pubmed-meshheading:19232330-Mutation, pubmed-meshheading:19232330-Neurons, pubmed-meshheading:19232330-Proto-Oncogene Proteins c-fos, pubmed-meshheading:19232330-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:19232330-Septal Nuclei, pubmed-meshheading:19232330-Social Behavior, pubmed-meshheading:19232330-Stress, Physiological, pubmed-meshheading:19232330-Swimming
pubmed:year
2009
pubmed:articleTitle
Neural activation deficits in a mouse genetic model of NMDA receptor hypofunction in tests of social aggression and swim stress.
pubmed:affiliation
Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. gduncan@med.unc.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural