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Adenosine release" refers to the cellular process whereby neurons—and under some conditions astrocytes—release endogenous adenosines into the extracellular space. This occurs either directly through equilibrative nucleoside transporters or indirectly via ATP breakdown followed by enzymatic conversion outside cells[1][2]. Extracellularly released adenosines act primarily through four G protein-coupled receptor subtypes—A1, A2A, A2B, and A3—to regulate synaptic transmission and provide feedback inhibition during periods of high neuronal activity or metabolic stress. While critical for neuromodulation and neuroprotection during events like seizures or ischemia/hypoxia,[5] this term does not refer to any single druggable protein but instead encompasses several mechanisms that control brain homeostasis through purinergic signaling pathways.[1][6]
Drugs modulate downstream effects by acting on: Adenosine receptors (A1, A2A, A2B, A3), which are G protein-coupled receptors; Enzymes involved in adenosinergic signaling/metabolism. No drugs act directly on the generic process called “adenosine release.”
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