[Abstract Title]. - Society for Neuroscience

myelin associated glycoprotein (MAG) and quaking (QKI), but little is known about the resulting
myelin deficits. Here, we examined the cingulum bundle and cingulate cortex in two putative
mouse models of dysmyelination, the MAG knockout, and the Quaking spontaneous mutant.
These mice have specific behavioral deficits, particularly in fine motor tasks. In these models,
we investigated the effect of alterations in myelin formation and oligodendrocyte deficits on
prefrontal neuronal integrity, white matter coherence and integrity, and neuronal organization. In
the MAG model, myelinated fiber density was assessed in the cingulum bundle and was found to
be unchanged compared to wildtype control mice. Diffusion anisotropy imaging of the same
mice also revealed unchanged fractional anisotropy in the cingulum. Advanced sterelogical tools
were used to investigate the density and distribution of oligodendrocytes in the cingulum, as
well, in both models.
Our results suggest that the effects of dysmyelination in the cingulum in these mutant mouse
models, if any, may be very subtle. In this context, we are conducting 3-dimensional analysis of
the dendritic and spine integrity of pyramidal cells in both models at different ages based on
preliminary observations in the MAG knockout showing an attrition of the basal dendritic tree at
3 months of age. Further ultrastructural studies may be necessary to pinpoint the precise
neuropathological alterations at the synaptic level.
Disclosures: M. Hoistad , None; D. Segal, None; D. Carpenter, None; C.Y. Tang, None; P.R.
Hof, None.
Poster
254. Schizophrenia: Mutant Animal Models
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 254.26/Y15
Topic: C.15.d. Schizophrenia: Mutant animal models
Support: NH&MRC Grant
Trust Australia Scholarship
Title: Behavioral endophenotypes and dysregulation of RGS4 gene expression in the PLC-β1
knockout mice
Authors: *C. E. MCOMISH 1,2 , E. BURROWS 2 , M. HOWARD 2 , A. J. HANNAN 2 ;
1 Developmental Neurosci., RFMH, NY, NY; 2 Howard Florey Inst., Melbourne, Australia
Abstract: The complexity of the genetics underlying schizophrenia is highlighted by the
multitude of molecular pathways which have been reported to be disrupted in the disorder