Quantitative trait loci modulate ventricular size in the mouse brain

Zygourakis, Corinna C.; Rosen, Glenn D.

doi:10.1002/cne.10697

Cited by 25 publications

(17 citation statements)

References 41 publications

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“…In support of this conclusion, analyses of wild-typerecombinantinbredstrainsofmice(www.genenetwork. org) showed no significant correlation between ventricular size (Zygourakis and Rosen, 2003) and behavioral phenotypic traits such as spontaneous activity or anxiety (Mathis et al, 1995;Brodkin et al, 1998;Gill et al, 2000;Gill and Boyle, 2005). In addition, rats with kaolin-induced hydrocephaly performed as well as controls in the Morris water maze (Del Bigio et al, 2003).…”

Section: Relative Proportions Of Dendritic Spines In Ophn1mentioning

confidence: 96%

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Loss of X-Linked Mental Retardation Gene Oligophrenin1 in Mice Impairs Spatial Memory and Leads to Ventricular Enlargement and Dendritic Spine Immaturity

Khelfaoui¹,

Denis²,

Galen³

et al. 2007

J. Neurosci.

127

163

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Loss of oligophrenin1 (OPHN1) function in human causes X-linked mental retardation associated with cerebellar hypoplasia and, in some cases, with lateral ventricle enlargement. In vitro studies showed that ophn1 regulates dendritic spine through the control of Rho GTPases, but its in vivo function remains unknown. We generated a mouse model of ophn1 deficiency and showed that it mimics the ventricles enlargement without affecting the cerebellum morphoanatomy. The ophn1 knock-out mice exhibit behavioral defects in spatial memory together with impairment in social behavior, lateralization, and hyperactivity. Long-term potentiation and mGluRdependant long-term depression are normal in the CA1 hippocampal area of ophn1 mutant, whereas paired-pulse facilitation is reduced. This altered short-term plasticity that reflects changes in the release of neurotransmitters from the presynaptic processes is associated with normal synaptic density together with a reduction in mature dendritic spines. In culture, inactivation of ophn1 function increases the density and proportion of immature spines. Using a conditional model of loss of ophn1 function, we confirmed this immaturity defect and showed that ophn1 is required at all the stages of the development. These studies show that, depending of the context, ophn1 controls the maturation of dendritic spines either by maintaining the density of mature spines or by limiting the extension of new filopodia. Altogether, these observations indicate that cognitive impairment related to OPHN1 loss of function is associated with both presynaptic and postsynaptic alterations.

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Section: Relative Proportions Of Dendritic Spines In Ophn1mentioning

confidence: 96%

“…We calculated the mean, SE, and confidence interval (␣ ϭ 0.05) for both genotypes. Ventricular dilatation was defined as a ratio Ͼ4.6% (Zygourakis and Rosen, 2003). The volumes of the brains, measured before slicing, were not different between the two genotypes.…”

Section: Measurement Of Brain and Ventricle Volumesmentioning

confidence: 99%

Loss of X-Linked Mental Retardation Gene Oligophrenin1 in Mice Impairs Spatial Memory and Leads to Ventricular Enlargement and Dendritic Spine Immaturity

Khelfaoui¹,

Denis²,

Galen³

et al. 2007

J. Neurosci.

127

163

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“…Digital images of mouse brain sections were obtained from the Mouse Brain Library (MBL, http:// www.mbl.org). MBL procedures for processing tissue have been described previously (http://www.mbl.org) (Zygourakis and Rosen, 2003). Briefly, selected animals were deeply anesthetized with Avertin (0.5-0.8 ml, intraperitoneally (i.p.))…”

Section: Subjectsmentioning

confidence: 99%

Quantitative trait loci linked to thalamus and cortex gray matter volumes in BXD recombinant inbred mice

et al. 2007

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To investigate whether there are separate or shared genetic influences on the development of the thalamus and cerebral cortex, we identified quantitative trait loci (QTLs) for relevant structural volumes in BXD recombinant inbred (RI) strains of mice. In 34 BXD RI strains and two parental strains (C57BL/ 6J and DBA/2J), we measured the volumes of the entire thalamus and cortex gray matter using point counting and Cavalieri's rule. Heritability was calculated using analysis of variance (ANOVA), and QTL analysis was carried out using WebQTL (http://www.genenetwork.org). The heritability of thalamus volume was 36%, and three suggestive QTLs for thalamus volume were identified on chromosomes 10, 11 and 16. The heritability of cortical gray matter was 43%, and four suggestive QTLs for cortex gray matter volume were identified on chromosomes 2, 8, 16 and 19. The genetic correlation between thalamus and cortex gray matter volumes was 0.64. Also, a single QTL on chromosome 16 (D16Mit100) was identified for thalamus volume, cortex gray matter volume and Morris water maze search-time preference (r ¼ 0.71). These results suggest that there are separate and shared genetic influences on the development of the thalamus and cerebral cortex.

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“…Quantitative trait locus (QTL) mapping using mice has been used to identify susceptibility genes for endophenotypes of schizophrenia, including ventricular size 55 and prepulse inhibition [56][57][58][59] in F 2 animals and chromosome substitution strains. However, the relatively small number of highly polymorphic alleles in these strains might not be optimal in identifying genes for complex diseases such as schizophrenia.…”

Section: Mouse Models Can Inform Study Of the Etiology Of Schizophreniamentioning

confidence: 99%

Translational Neuroscience of Schizophrenia: Seeking a Meeting of Minds Between Mouse and Man

et al. 2011

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CitationTranslational neuroscience of Schizophrenia: seeking a meeting of minds between mouse and man. 2011, 3 AbstractUnderstanding the etiology of developmental brain disorders such as schizophrenia is critical for achieving advances in treatment and requires novel research strategies that control for individual variation in genetic background, environmental challenges and expression of phenotype. SYSGENET, a European systems genetics

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Quantitative trait loci modulate ventricular size in the mouse brain

Cited by 25 publications

References 41 publications

Loss of X-Linked Mental Retardation Gene Oligophrenin1 in Mice Impairs Spatial Memory and Leads to Ventricular Enlargement and Dendritic Spine Immaturity

Loss of X-Linked Mental Retardation Gene Oligophrenin1 in Mice Impairs Spatial Memory and Leads to Ventricular Enlargement and Dendritic Spine Immaturity

Quantitative trait loci linked to thalamus and cortex gray matter volumes in BXD recombinant inbred mice

Translational Neuroscience of Schizophrenia: Seeking a Meeting of Minds Between Mouse and Man

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