Oligodendrocytes are produced from the same region of the ventral spinal cord that earlier generated motor neurons in bird and rodent embryos. Motor neuron and oligodendrocyte precursor cells express Olig genes, which encode basic helix-loop-helix transcription factors that play important roles in the development of both motor neurons and oligodendrocytes. We found that oligodendrocytes develop similarly in zebrafish embryos, in that they arise from ventral spinal cord and migrate to new positions. Developing primary motor neurons and oligodendrocytes express olig2 as do neural plate cells that give rise to both primary motor neurons and oligodendrocytes. Loss of olig2 function prevented primary motor neuron and oligodendrocyte development, whereas olig2 overexpression promoted formation of excess primary motor neurons and oligodendrocytes. We provide genetic evidence that Hedgehog signaling is required for zebrafish olig2 expression and oligodendrocyte development. However, olig2 overexpression did not promote primary motor neuron or oligodendrocyte development in embryos with reduced Hedgehog signaling activity. One possibility consistent with these data is that Hedgehog signaling, partly by inducing olig2 expression, specifies neural precursor cells that have potential for primary motor neuron or oligodendrocyte fate.

Fragile-X syndrome is a common form of mental retardation resulting from the inability to produce the fragile-X mental retardation protein. The specific function of this protein is unknown; however, it has been proposed to play a role in developmental synaptic plasticity. Examination of human brain autopsy material has shown that fragile-X patients exhibit abnormalities in dendritic spine structure and number, suggesting a failure of normal developmental dendritic spine maturation and pruning in this syndrome. Similar results using a knockout mouse model have previously been described; however, it was noted in retrospect that the mice used in that study may have carried a mutation for retinal degeneration, which may have affected cell morphology in the visual cortex of those animals. In this study, dendritic spines on layer V pyramidal cells of visual cortices, taken from fragile-X knockout and wild-type control mice without the retinal degeneration mutation and stained using the Golgi-Cox method, were investigated for comparison with the human condition. Quantitative analyses of the lengths, morphologies, and numbers of dendritic spines, as well as amount of dendritic arbor and dendritic branching complexity, were conducted. The fragile-X mice exhibited significantly more long dendritic spines and significantly fewer short dendritic spines than control mice. Similarly, fragile-X mice exhibited significantly more dendritic spines with an immature-like morphology and significantly fewer with a more mature type morphology. However, unlike the human condition, fragile-X mice did not exhibit statistically significant dendritic spine density differences from controls. Fragile-X mice also did not demonstrate any significant differences from controls in dendritic tree complexity or dendritic arbor. Long dendritic spines with immature morphologies are characteristic of early development or a lack of sensory experience. These results are similar to those found in the human condition and further support a role for the fragile-X mental retardation protein specifically in normal dendritic spine developmental processes. They also support the validity of these mice as a model of fragile-X syndrome.

Earthquake phenomenology exhibits a number of power law distributions including the Gutenberg-Richter frequency-size statistics and the Omori law for aftershock decay rates. In search for a basic model that renders correct predictions on long spatiotemporal scales, we discuss results associated with a heterogeneous fault with long-range stress-transfer interactions. To better understand earthquake dynamics we focus on faults with Gutenberg-Richter-like earthquake statistics and develop two universal scaling functions as a stronger test of the theory against observations than mere scaling exponents that have large error bars. Universal shape profiles contain crucial information on the underlying dynamics in a variety of systems. As in magnetic systems, we find that our analysis for earthquakes provides a good overall agreement between theory and observations, but with a potential discrepancy in one particular universal scaling function for moment rates. We primarily use mean field theory for the theoretical analysis, since it has been shown to be in the same universality class as the full three-dimensional version of the model (up to logarithmic corrections). The results point to the existence of deep connections between the physics of avalanches in different systems.

In order to test if the universal aspects of Barkhausen noise in magnetic materials can be predicted from recent variants of the non-equilibrium zero temperature Random Field Ising Model (RFIM), we perform a quantitative study of the universal scaling function derived from the Barkhausen pulse shape in simulations and experiment. Through data collapses and scaling relations we determine the critical exponents τ and 1/σνz in both simulation and experiment. Although we find agreement in the critical exponents, we find differences between theoretical and experimental pulse shape scaling functions as well as between different experiments.

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