Locomotor recovery following contusive spinal cord injury does not require oligodendrocyte remyelination

The contribution of oligodendrocytes to remyelination in functional recovery after spinal cord injury is not fully understood. Here, the authors show that oligodendrocyte progenitor cell differentiation is not required for functional recovery after spinal cord injury in mice

Contrast-associated transient cortical blindness: three cases with MRI and electrophysiology findings

Transient cortical blindness (TCB) is a rare but striking complication following contrast agent injection. TCB might be secondary to a direct toxicity of the contrast agent, leading to an osmotic disruption of the blood-brain barrier (BBB), with a preferential involvement of the posterior circulation and occipital cortex. We report a series of three patients with contrast medium-associated TCB (intra-arterial injection of non-ionic contrast agent during diagnostic cerebral angiography for two of them and coronary angioplasty for the other one). In two patients, the magnetic resonance imaging (MRI) was unremarkable; in the other patient, typical MRI findings were observed, with FLAIR hyperintensities in the right occipital cortex and decreased apparent diffusions coefficient (ADC). Interestingly, this patient also presented posterior rhythmic epileptiform activities on electroencephalogram during the first 36 h. Visual evoked potentials (VEPs) showed normal retinal potential, but a massive destructuration of the later potentials of the cortical origin. To our knowledge, this is the first time that VEPs acquired during TCB are reported. We discuss these findings with respect to the pathophysiology of TCB

EphB3 receptors function as dependence receptors to mediate oligodendrocyte cell death following contusive spinal cord injury

We demonstrate that EphB3 receptors mediate oligodendrocyte (OL) cell death in the injured spinal cord through dependence receptor mechanism. OLs in the adult spinal cord express EphB3 as well as other members of the Eph receptor family. Spinal cord injury (SCI) is associated with tissue damage, cellular loss and disturbances in EphB3-ephrinB3 protein balance acutely (days) after the initial impact creating an environment for a dependence receptor-mediated cell death to occur. Genetic ablation of EphB3 promotes OL survival associated with increased expression of myelin basic protein and improved locomotor function in mice after SCI. Moreover, administration of its ephrinB3 ligand to the spinal cord after injury also promotes OL survival. Our in vivo findings are supported by in vitro studies showing that ephrinB3 administration promotes the survival of both oligodendroglial progenitor cells and mature OLs cultured under pro-apoptotic conditions. In conclusion, the present study demonstrates a novel dependence receptor role of EphB3 in OL cell death after SCI, and supports further development of ephrinB3-based therapies to promote recovery

Regenerating CNS myelin — from mechanisms to experimental medicines

Although the core concept of remyelination - based on the activation, migration, proliferation and differentiation of CNS progenitors - has not changed over the past 20 years, our understanding of the detailed mechanisms that underlie this process has developed considerably. We can now decorate the central events of remyelination with a host of pathways, molecules, mediators and cells, revealing a complex and precisely orchestrated process. These advances have led to recent drug-based and cell-based clinical trials for myelin diseases and have opened up hitherto unrecognized opportunities for drug-based approaches to therapeutically enhance remyelination