Currently our research is focused on the study of neuron-glial communication as a therapeutic strategy in demyelinating scenarios. In the laboratory, we employ several strategies for the approach in this context, mainly using animal models with damage or alterations of focal demyelination (by stereotaxic injection of gliotoxins) or systemic (cuprizone model, hypoxia in the postnatal stage) and these approaches are monitored transversely by histology, and also longitudinally using magnetic resonance imaging. We are currently investigating the role of oligodendroglial GABAergic signaling in myelination and the feasibility of modulating this signaling to enhance GABA type A receptor activity and, possibly, remyelination.