Neuron-Glia signaling in synaptic plasticity: Astrocytes Rule!

Abstract

Astrocytes are increasingly being recognized as active players for neuronal synaptic communication, with multiple functions for central nervous system physiology. Nevertheless, astrocytes are typically considered as modulators of core mechanisms driven by the neuronal function (for instance by relulating neurovascuscular-neuroenergetic coupling). We will discuss new conclusive evidences that challenge this view, specifically for a form of synaptic plasticity involved in cognitive function: NMDA receptor-dependent long- term depression (LTD) in the hippocampus. Even though the molecular mechanisms for LTD are still being elucidated, the basic sequence of events that leads to synaptic depression appears to be well stablished (and widely accepted): prolonged, low-frequency release of glutamate from the presynaptic terminal, activation of postsynaptic NMDA receptors and engagement of specific signaling cascades that lead to the removal of AMPA receptors from the postsynaptic membrane. I will present a fundamental change of paradigm, in which the axis composed of presynaptic neuron-astrocyte-postsynaptic neuron defines an obligatory relay for information processing leading to synaptic plasticity.