Topic: gliotransmission

Alzheimer’s disease (AD) is characterized by a long asymptomatic phase associated with the toxic accumulation of oligomeric form of amyloid-beta peptide (Aβo). One of the first event reported in this phase seems to be a specific hippocampal hyperactivity in both humans and AD mouse model. We highlighted that this early hyperactivity starts with an abnormal increase of calcium activity in astrocytes which affects neighbouring neurons in the hippocampus. We identified an astrocytic calcium channel, transient receptor potential ankyrin-1 (TRPA1), implicated in the Aβo-induced hippocampal hyperact

In recent years, a pivotal role of gliotransmission in homeostatic synaptic plasticity has been highlighted and glial-derived ATP arises as a key contributor. However, very little is known about the glial non-vesicular ATP-release pathway and how ATP participates in the modulation of synaptic strength. In this work, we have analyzed the functional changes occurring in neurons upon chronic activity blockade and the role of the purinergic signaling, connexin43 and pannexin1 hemichannels in this process. By using hippocampal dissociated cultures, we showed that blocking connexin43 and pannexin1 h