Astrocyte-neuron interplay in maladaptive plasticity.

The complexity of neuronal networks cannot only be explained by neuronal activity so neurobiological research in the last decade has focused on different components of the central nervous system: the glia. Glial cells are fundamental elements for development and maintenance of physiological brain work. New data confirm that glia significantly influences neuronal communication through specific molecules, named "gliotransmitters", and their related receptors. This new approach to the traditional model of the way synapses work is also supported by changes occurring in pathological conditions, such as neurodegenerative diseases or toxic/traumatic injury to nervous system. Experimental models have revealed that glial cells are the starting point of damage progression that subsequently involves neurons. The "bedside to bench" approach has demonstrated that clinical phenotypes are strictly related to neuronal death, however it is conceivable that the disease begins earlier, years before clinical onset. This temporal gap is necessary to determine complex changes in the neuro-glial network organization and produce a "maladaptive plasticity". We review the function of glial cells in health and disease, pointing the putative mechanisms of maladaptive plasticity, suggesting that glial cells may represent a fascinating therapeutic target to prevent irreversible neuronal cell death.