Fig. (1).
A schematic model of the interaction of P2X7, CB1 and A1 receptors located on glutamatergic terminals. Activation of P2X7 receptors facilitate and those of A1 receptors reduces the release of glutamate. Glutamate (Glu) released into synaptic gap activates AMPA and NMDA receptors on the postsynaptic site. ATP released from astrocytes [20] and microglia [172] acts on P2X7 receptors located on the terminal of glutamatergic neurons and facilitates the release of Glu ([173] for review see [174]). Adenosine decomposed from ATP acts on A1 receptors inhibiting the release of Glu [168, 175]. This inhibitory effect of A1 receptor activation may be mediated by inhibiting voltage-dependent Ca2+ channels, which reduces Ca transients measured in the bouton [176]. CB1 cannabinoid receptors together with A1 receptors are also expressed on glutamatergic terminals [80] and activation of both of these receptors results in a decrease of Glu release. Extremely high concentrations of adenosine act on A2A receptors to increase the release of Glu [77].