title: Oxytocin receptors in brain cortical regions are reduced in haploinsufficient (+/-) reeler mice.
abstract: OBJECTIVE
  Both oxytocin (OT) and reelin are particularly significant during development and the absence of either may interfere with normal brain development. In addition, reelin is critical to the development of the GABAergic system and GABA modulates the release of OT. Availability of the reelin haploinsufficient (+/-) reeler mouse (HRM) provides a model for examining the role of reelin in the development of the OT system and especially in the expression of the OT receptor (OTR).
  
  
  METHODS
  In this study we used immunocytochemistry and in situ hybridization in HRM versus wild-type (+/-) mice (WTM) to quantify OTR abundance in regions of the brain cortex.
  
  
  RESULTS
  Our findings reveal that the oxytocin receptor (OTR), measured either by immunohistochemistry or in situ hybridization, is significantly lower in HRM. Areas showing significant deficits included the piriform cortex, neocortex, retrosplenial cortex and certain regions of the hippocampus.
  
  
  CONCLUSIONS
  Both reelin and OT play a role in regulating affect and mood. Down-regulation of reelin has been strongly correlated with schizophrenia and it is proposed that HRM may serve as a model for neural deficits seen in both schizophrenia and autism. We report that HRM show regionally specific reductions in OTRs, especially in cortical areas, which previously have been implicated in social memory and cognitive functions. These findings offer support for the more general hypothesis that down-regulation of reelin, of either genetic or epigenetic origin, through associated reductions in the OTRs, contributes to the deficiencies in social behavior that are characteristic of both schizophrenia and autism.
authors.affiliation: Department of Psychiatry, University of Illinois at Chicago, 1601 W. Taylor Street, Chicago, IL 60612, USA.
authors.forename: Wensheng
authors.initials: W
authors.lastname: Liu
authors.forename: George D
authors.initials: GD
authors.lastname: Pappas
authors.forename: C Sue
authors.initials: CS
authors.lastname: Carter
mesh_terms: D000818:Animals; D001921:Brain / Q000033:anatomy & histology / Q000378:metabolism*; D015816:Cell Adhesion Molecules, Neuronal / Q000172:deficiency*; D002452:Cell Count / Q000379:methods; D016326:Extracellular Matrix Proteins / Q000172:deficiency*; D005786:Gene Expression Regulation / Q000502:physiology; D006579:Heterozygote; D007150:Immunohistochemistry / Q000379:methods; D017403:In Situ Hybridization / Q000379:methods; D051379:Mice; D018345:Mice, Knockout; D008818:Mice, Neurologic Mutants; D009419:Nerve Tissue Proteins / Q000172:deficiency*; D012333:RNA, Messenger / Q000378:metabolism; D018045:Receptors, Oxytocin / Q000235:genetics / Q000378:metabolism*; D000091042:Reelin Protein; D012697:Serine Endopeptidases / Q000172:deficiency*
chemical_list: D015816:Cell Adhesion Molecules, Neuronal; D016326:Extracellular Matrix Proteins; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D018045:Receptors, Oxytocin; D000091042:Reelin Protein; C000717128:Reln protein, mouse; D012697:Serine Endopeptidases