Modulation of Central Synapses by Astrocyte-Released ATP and Postsynaptic P2X Receptors

Figure 1

Summary of the postsynaptic P2X-mediated modulation of synaptic strength and plasticity following the release of ATP by astrocytes or neurons. Glutamate and noradrenaline acting on astrocytes cause the release of glial ATP. Activation of postsynaptic P2X receptors at glutamatergic synapses (blue) can trigger either a PIK3-dependent insertion of AMPAR leading to the increase of synaptic strength and synapse scaling (left) or a CaMKII-dependent internalization of AMPAR leading to a P2X-dependent synaptic depression (middle). P2X receptors can also cause an alteration of glutamatergic synapse plasticity by inhibiting NMDA function by interfering on PSD-95/NMDAR complex. At inhibitory synapses (brown), glial or neuronal ATP decreases GABAergic synapse efficacy by direct or indirect alteration of GABA_A (right).