Abstract
BackgroundMecp2 null mice model Rett syndrome (RTT) a human neurological disorder affecting females after apparent normal pre- and peri-natal developmental periods. Neuroanatomical studies in cerebral cortex of RTT mouse models revealed delayed maturation of neuronal morphology and autonomous as well as non-cell autonomous reduction in dendritic complexity of postnatal cortical neurons. However, both morphometric parameters and high-resolution expression profile of cortical neurons at embryonic developmental stage have not yet been studied. Here we address these topics by using embryonic neuronal primary cultures from Mecp2 loss of function mouse model.ResultsWe show that embryonic primary cortical neurons of Mecp2 null mice display reduced neurite complexity possibly reflecting transcriptional changes. We used RNA-sequencing coupled with a bioinformatics comparative approach to identify and remove the contribution of variable and hard to quantify non-neuronal brain cells present in our in vitro cell cultures.ConclusionsOur results support the need to investigate both Mecp2 morphological as well as molecular effect in neurons since prenatal developmental stage, long time before onset of Rett symptoms.Electronic supplementary materialThe online version of this article (doi:10.1186/s12859-015-0859-7) contains supplementary material, which is available to authorized users.
Highlights
methyl CpG binding protein 2 (Mecp2) null mice model Rett syndrome (RTT) a human neurological disorder affecting females after apparent normal pre- and peri-natal developmental periods
Mecp2 deficiency impairs primary branching of embryonic cortical neurons We examined primary cultures of neurons dissected from embryonic day 15 (E15) cerebral cortices of Mecp2 null embryos (Mecp2tm1.1Bird/J strain) to investigate whether changes in neuronal morphology already occur during early brain development of RTT mouse models
More than 90 % of cortical cells in wild type (WT) and Mecp2 null mouse cultures were neurons, as judged by counting the Tuj1 positive cells counterstained with the nuclear marker DAPI (Fig. 1)
Summary
Mecp null mice model Rett syndrome (RTT) a human neurological disorder affecting females after apparent normal pre- and peri-natal developmental periods. Neuroanatomical studies in cerebral cortex of RTT mouse models revealed delayed maturation of neuronal morphology and autonomous as well as non-cell autonomous reduction in dendritic complexity of postnatal cortical neurons. Both morphometric parameters and highresolution expression profile of cortical neurons at embryonic developmental stage have not yet been studied. We address these topics by using embryonic neuronal primary cultures from Mecp loss of function mouse model.
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