{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T23:54:03Z","timestamp":1775087643029,"version":"3.50.1"},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1987,3,1]],"date-time":"1987-03-01T00:00:00Z","timestamp":541555200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1987,3]]},"abstract":"<jats:p>1. The effects of adenosine deaminase, inosine, alkylxanthines (8\u2010phenyltheophylline (8\u2010PT), theophylline and isobutylmethylxanthine (IBMX], dipyridamole, alpha, beta\u2010methylene ADP (AOPCP) and ATP analogues (alpha, beta\u2010methylene ATP and beta, gamma\u2010methylene ATP) on evoked end\u2010plate potentials (e.p.p.s) were investigated in innervated sartorius muscles of the frog, in which twitches had been prevented with tubocurarine. The effects of 8\u2010PT and IBMX on the amplitude and quantal content of e.p.p.s were also investigated in innervated sartorius muscles of the frog, in which twitches had been prevented with high\u2010magnesium solutions. 2. Adenosine deaminase reversibly increased the amplitude of e.p.p.s and prevented the reduction caused by exogenously applied adenosine on e.p.p. amplitude. The increase caused by adenosine deaminase was equivalent to the decrease caused by 12 +\/\u2010 5.8 microM\u2010adenosine on e.p.p. amplitude. 3. Inosine, the product of adenosine deamination, was virtually devoid of effect on e.p.p.s. 4. The adenosine receptor antagonists at the frog neuromuscular junction, 8\u2010PT and theophylline, increased in a concentration\u2010dependent manner the amplitude of e.p.p.s in the presence of tubocurarine. 8\u2010PT increased the amplitude and quantal content of e.p.p.s in the presence of high magnesium. IBMX, which does not behave as an adenosine receptor antagonist at the frog neuromuscular junction, decreased the amplitude of e.p.p.s in the presence of tubocurarine or high\u2010magnesium solutions. 5. Dipyridamole, an adenosine uptake blocker, decreased the amplitude of e.p.p.s, and in a concentration that did not affect neuromuscular transmission potentiated the depressing effect of adenosine, but not that of 2\u2010chloroadenosine, on the amplitude of e.p.p.s. 6. AOPCP, an inhibitor of 5'\u2010nucleotidase, increased the amplitude of e.p.p.s and markedly attenuated the depressing effect of ATP, but not that of adenosine, on e.p.p. amplitude. 7. The ATP analogue, alpha, beta\u2010methylene ATP, which is not a substrate for 5'\u2010nucleotidase, was virtually devoid of effect on e.p.p.s. beta, gamma\u2010Methylene ATP, which can be a substrate for 5'\u2010nucleotidase, mimicked the depressing effect of ATP on e.p.p. amplitude, an effect which was also reduced by AOPCP. 8. It is concluded that in conditions in which the initial quantal content is assumed to be normal (1) endogenous adenosine depresses neuromuscular transmission, (2) at the neuromuscular junction adenosine is inactivated through a dipyridamole\u2010sensitive uptake process, and (3) released adenine nucleotides might contribute to the pool of endogenous adenosine which modulates neuromuscular transmission.<\/jats:p>","DOI":"10.1113\/jphysiol.1987.sp016470","type":"journal-article","created":{"date-parts":[[2014,12,19]],"date-time":"2014-12-19T06:42:16Z","timestamp":1418971336000},"page":"571-585","source":"Crossref","is-referenced-by-count":120,"title":["On the role, inactivation and origin of endogenous adenosine at the frog neuromuscular junction."],"prefix":"10.1113","volume":"384","author":[{"given":"J A","family":"Ribeiro","sequence":"first","affiliation":[]},{"given":"A M","family":"Sebasti\u00e3o","sequence":"additional","affiliation":[]}],"member":"311","published-online":{"date-parts":[[1987,3]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1987.sp016470","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1987.sp016470","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,20]],"date-time":"2023-10-20T14:23:04Z","timestamp":1697811784000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1987.sp016470"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1987,3]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1987,3]]}},"alternative-id":["10.1113\/jphysiol.1987.sp016470"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1987.sp016470","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1987,3]]}}}