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Arlotta, P. et al. Neuronal subtype-specific genes that control corticospinal motor neuron development in vivo.
Motility effects of p27 may exist in normal cells, since p27-dependent migration is essential for normal cortical neuron development in vivo in murine embryos [ 33, 34].
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Our results represent the first report on the electrophysiology of SMN-deficient motor neurons, and suggest that motor neuron development in vitro follows a different path than in vivo development, a path in which loss of SMN expression has little effect on motor neuron function and survival.
These results represent the first report of the electrophysiological properties of spinal motor neurons from an SMN-deficient model organism, and suggest that motor neuron development in vitro follows a developmental path in which motor neuron function and survival is much less dependent on SMN expression than in vivo development.
The lack of dependence of cultured motor neurons on SMN expression indicates that care must be taken in using motor neuron culture as a model system for studying SMA, but also suggests that a deeper understanding of how motor neuron development in culture differs from development in vivo may provide key insights into the pathophysiology of SMA.
Taken together, these results suggest that motor neuron development in culture proceeds down a different developmental pathway than in vivo development in the spinal cord, and that in vitro development leads to motor neurons that are much less dependent on expression of SMN for survival and function.
Loss of Ctip1 function results in a striking bias in favor of subcerebral projection neuron development in sensory cortex at the expense of corticothalamic and deep-layer callosal development, while misexpression of Ctip1 in vivo represses subcerebral gene expression and projections.
Firstly, using immunocytochemistry, we confirmed GITRL and GITR expression in cultured neonatal mouse SCG neurons, which is a period of development in vivo when these neurons are undergoing extensive growth and branching within their peripheral targets.
RORγtM supports thymocyte development in vivo.
Collectively, these data establish the requirement of RING tetramerization in APL development in vivo and arsenic response ex vivo.
The current study examined the expression of C9ORF72 in the mouse CNS over development in vivo and in vitro in order to provide information about its expression and cellular localization during neurite outgrowth, neuron maturation and synapse formation.
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