1. Glial Development: The Crossroads of Regeneration and Repair in the CNS 
Vittorio Gallo, Benjamin Deneen 
Neuron 
Volume 83, Issue 2, Pages (July 2014)
DOI: /j.neuron
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2. Figure 2 Astrocyte Roads to Reactivity
The two key processes associated with astrocyte development that directly contribute to the reactive astrocyte phenotype are proliferation and GFAP-induction. Molecular regulation of these processes during development is viewed as the road to astrocyte reactivity and understanding how they are recapitulated after injury will serve as a starting point for understanding the nature of reactive astrocytes.
Neuron  , DOI: ( /j.neuron )
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3. Figure 1 Development of the Astrocyte Lineage
Schematic synopsis of the cellular and molecular processes that oversee the specification and differentiation of the astrocyte lineage. Unlike neuronal- or oligodendrocyte-lineage development, the intermediate stages of astrocyte lineage development remain poorly defined, due in part, to the lack of reliable markers and clearly defined functional endpoints.
Neuron  , DOI: ( /j.neuron )
Copyright © 2014 Elsevier Inc. Terms and Conditions

4. Figure 3
Positive and Negative Regulators of Oligodendrocyte Development and Regeneration
Schematic synopsis of the major developmental phases of oligodendrocyte maturation—i.e., proliferation, cell-cycle exit/differentiation and myelination—after demyelination of the adult brain. Green arrows refer to enhancers of these processes under pathological conditions, whereas red arrows refer to inhibitory pathways. Preventing or suppressing the inhibitory effects of specific pathways, as well as leveraging on enhancers promotes oligodendrocyte maturation and myelination and might define future cell-based therapeutic approaches to demyelinating diseases.
Neuron  , DOI: ( /j.neuron )
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5. Figure 4
Oligodendrocyte Regeneration through Lineage Plasticity of GAD-Expressing Neuroblasts
Demyelination of the adult white matter (corpus callosum) causes fate plasticity in GAD-expressing (GAD+) neuroblasts of the subventricular zone (SVZ). Under normal physiological conditions, Olig2 expression is repressed by BMP signaling in GAD+ neuroblasts. Demyelination causes upregulation in the levels of the BMP antagonist chordin in the SVZ, which prevents BMP signaling and results in induction of Olig2 expression in GAD+ cells. These cells migrate out of the SVZ into the corpus callosum, where they generate mature, myelinating oligodendrocytes (see Jablonska et al., 2010).
Neuron  , DOI: ( /j.neuron )
Copyright © 2014 Elsevier Inc. Terms and Conditions