title: Increased acetylcholine content induced by antidromic stimulation of a sympathetic ganglion: a possible retrograde action of adenosine.
abstract: Prolonged high-frequency orthodromic stimulation of superior cervical ganglia is known to result in increased acetylcholine (ACh) synthesis and ACh content after the period of stimulation. In a previous study, we provided evidence to suggest that adenosine acts as an extracellular signal to activate this increased ACh synthesis and we proposed that the source of that adenosine might be postsynaptic. Thus, the purpose of the present study was to test whether direct stimulation of the post-ganglionic nerves could affect ganglionic ACh content. Antidromic conditioning of ganglia (15 Hz, 45 min) did not affect significantly their ACh content. However, if ganglia were allowed a 15-min rest period after this antidromic conditioning, their ACh stores were increased by 20%; a similar increase was induced by 4-Hz stimulation before the rest period. During the 15-Hz antidromic stimulation, ACh release was not clearly increased above the basal level, suggesting that preganglionic nerve endings were not stimulated to an extent that could explain the increased ACh content. Orthodromic stimulation (5 Hz) of ganglia 15 min after they had been subjected to antidromic conditioning (15 Hz, 45 min) showed increased ACh release in comparison with that from control unconditioned ganglia. Moreover, the extra ACh released by the conditioned ganglia was quantitatively similar to the increase in the ACh stores, as if most, or all, of the additional ACh was released by preganglionic stimulation. If the antidromic conditioning and the rest period were done during perfusion with Ca(2+)-free medium, the ganglia did not accumulate extra ACh.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada.
authors.forename: A
authors.initials: A
authors.lastname: Tandon
authors.forename: B
authors.initials: B
authors.lastname: Collier
mesh_terms: D000109:Acetylcholine / Q000378:metabolism*; D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002352:Carrier Proteins / Q000037:antagonists & inhibitors; D002415:Cats; D003470:Culture Media / Q000378:metabolism; D004176:Dipyridamole / Q000494:pharmacology; D004558:Electric Stimulation; D005260:Female; D005728:Ganglia, Sympathetic / Q000502:physiology*; D008297:Male; D008565:Membrane Proteins / Q000037:antagonists & inhibitors; D033703:Nucleoside Transport Proteins; D013868:Thioinosine / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D002352:Carrier Proteins; D003470:Culture Media; D008565:Membrane Proteins; D033703:Nucleoside Transport Proteins; D013868:Thioinosine; D004176:Dipyridamole; C001789:4-nitrobenzylthioinosine; D000241:Adenosine; D000109:Acetylcholine; D002118:Calcium