“…Pre-clinical studies pointed out an inhibitory effect exerted by adenosine, via A 1 receptor activation, on pain transmission both at pre-synaptic level, counteracting the pain-associated neurotransmitter release, such as glutamate, calcitonin gene-related peptide and substance P, and at post-synaptic level, through membrane cell hyperpolarization (68,69). Sohn et al reported that the intrathecal administration of the A 1 receptor agonist R-PIA, but not the A 2A receptor agonist CGS-21680 hydrochloride, decreased the visceromotor responses (70). Currently, some authors paid greater attention to the potential anti-nociceptive effects of A 3 agonists (71,72).…”