Topic: oligodendrogenesis

Developmental myelination is a protracted process in the mammalian brain. One theory for why oligodendrocytes mature so slowly posits that myelination may stabilize neuronal circuits and temper neuronal plasticity as animals age. We tested this theory in the visual cortex, which has a well-defined critical period for experience-dependent neuronal plasticity. During adolescence, visual experience modulated oligodendrocyte maturation in visual cortex. To determine whether oligodendrocyte maturation in turn regulates neuronal plasticity, we genetically blocked oligodendrocyte differentiation and

Oligodendrocytes, the myelinating glial cells of the central nervous system (CNS), surround axons with their membrane extensions, forming the myelin sheath. Loss of oligodendrocytes and/or myelin (demyelination) occurs in traumatic brain injury or pathologies such as multiple sclerosis. Since, there is no specific treatment for demyelination; we are interested in enhancing myelin endogenous repair. We focus our work on A Disintegrin and Metalloprotease (ADAM) 10, the major CNS α-secretase, which generates the neuroprotective soluble fragment sAPPα via cleavage of the Amyloid Precursor Protein

Oligodendrocytes (OLs) are the myelin-forming cells in the Central Nervous System of vertebrates. The role of Adenosine A2A receptors (A2ARs) and brain-derived neurotrophic factor (BDNF) on adult oligodendrogenesis from subventricular zone neural stem cells (SVZ-NSCs) remains highly unknown. We aimed at studying how these modulators and their putative crosstalk impact OL differentiation from postnatal SVZ-NSCs. For this, C57BL/6 P1-3 mice SVZ-derived neurospheres were pharmacologically exposed to BDNF (30 ng/mL) and ZM 241385 (50 nM), an antagonist for A2ARs. mRNA expression levels of oligoden