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Thus, if in peripheral tissues adenosine mediates anti-inflammatory effects through A2A receptors, in the case of neuroinflammation, the activation of these receptors is responsible for neuronal degradation [89] through the influence exerted on glial cells, which involves the stimulation of cyclooxygenase type 2 (COX2), nitric oxide synthase (NOS), the release of prostaglandins, cytokines, and stimulation of Glu efflux from the presynaptic level [90,91,92]