Stimulation of the adenosine A3 receptor, not the A1 or A2 receptors, promote neurite outgrowth of retinal ganglion cells

Experimental Eye Research
Kei-Ichi NakashimaHidenobu Tanihara

Abstract

Among candidate neuroprotective agents, adenosine is thought to be a possible treatment for central nervous system disorders. Adenosine elicits biological effects through four G protein-coupled receptors (A1, A2A, A2B, and A3). The A2A and A2B receptors stimulate adenylyl cyclase (AC) and increase cyclic adenosine monophosphate (cAMP) levels, whereas A1 and A3 receptors inhibit AC and decrease cAMP levels. Several studies have investigated the effects of adenosine receptors (AdoRs) in glaucoma, because modulation of A1, A2A, or A3 receptor regulates intraocular pressure. In addition, AdoR-related phenomena may induce neuroprotective effects in retinal neurons. Notably, A1, A2A, and A3 receptor agonists reportedly inhibit retinal ganglion cell (RGC) death in in vitro and in vivo glaucoma models. However, there is limited knowledge of the effects of AdoR activation on neurite outgrowth or the regeneration of RGCs. In this report, we described the role of an AdoR subtype in neurite outgrowth and RGC axonal regeneration. The distribution of AdoRs in the retina was evaluated by immunohistochemical analysis. Using primary cultured rat RGCs in vitro and an optic nerve crush model in vivo, neurite elongation was evaluated after stimula...Continue Reading

Citations

Mar 29, 2020·International Journal of Molecular Sciences·Raquel BoiaAna Raquel Santiago
Jul 6, 2019·Purinergic Signalling·Stephanie L GrilloSalvatore L Stella
Oct 4, 2020·International Journal of Molecular Sciences·Joana Ferreira-SilvaAna Raquel Santiago
Dec 14, 2018·Frontiers in Neuroscience·Marita Pietrucha-DutczakAdrian Smedowski
Dec 12, 2020·Free Radical Biology & Medicine·Camila C PortugalRoberto Paes-de-Carvalho

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