Adenosine analogs inhibit acetylcholine release and cyclic AMP synthesis in the guinea-pig superior cervical ganglion

• Published in: Neuroscience letters 1995-01, Vol.184 (2), p.97-100
• Main Authors: Giorgio Borasio, Pier, Pavan, Barbara, Fabbri, Elena, Ginanni-Corradini, Federica, Arcelli, Diego, Poli, Alessandro
• Format: Article
• Language: English
• Subjects: Acetylcholine - metabolism; Acetylcholine release; Adenosine - analogs & derivatives; Adenosine - pharmacology; Adenosine A1-receptor; Adenosine analogs; Animals; Biological and medical sciences; Colforsin - pharmacology; Cyclic AMP; Cyclic AMP - biosynthesis; Depression, Chemical; Electric Stimulation; Fundamental and applied biological sciences. Psychology; Guinea Pigs; Guinea-pig superior cervical ganglion; Imidazoles - pharmacology; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ; Phosphodiesterase Inhibitors - pharmacology; Presynaptic Terminals - drug effects; Presynaptic Terminals - metabolism; Purinergic P1 Receptor Agonists; Purinergic P1 Receptor Antagonists; Superior Cervical Ganglion - drug effects; Superior Cervical Ganglion - metabolism; Sympathetic Nervous System - physiology; Vertebrates: nervous system and sense organs; Xanthines - pharmacology
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/0304-3940(94)11178-L

The ability of adenosine agonists to modulate the electrically evoked release of acetylcholine (ACh) from [ 3H]choline preloaded guinea-pig superior cervical ganglia (SCG) was investigated. The adenosine A1-receptor selective agonist N 6-cyclohexyladenosine (CHA) and 2-chloroadenosine (2-CADO) inhibited the evoked transmitter release, the effect being reversed by the A1-receptor selective antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), and by sulmazole (SUL), which blocks both the A1-receptor and the adenylate cyclase inhibitory regulator Gi. In whole ganglia, CHA decreased both the basal and the forskolin (FSK)-stimulated cyclic AMP synthesis. The latter effect was again prevented by the A1 antagonist DPCPX. These results are compatible with the existence, in the guinea-pig SCG, of adenosine A1-receptors, part of which are located on the presynaptic nerve terminals mediating an inhibition of ACh release.