{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T01:53:14Z","timestamp":1789609994550,"version":"build-2803163510"},"reference-count":48,"publisher":"Wiley","issue":"23","license":[{"start":{"date-parts":[[2009,1,7]],"date-time":"2009-01-07T00:00:00Z","timestamp":1231286400000},"content-version":"vor","delay-in-days":37,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2008,12]]},"abstract":"<jats:p>Spontaneous purinergic neurotransmission was characterized in the mouse urinary bladder, a model for the pathological or ageing human bladder. Intracellular electrophysiological recording from smooth muscle cells of the detrusor muscle revealed spontaneous depolarizations, distinguishable from spontaneous action potentials (sAPs) by their amplitude (&lt; 40 mV) and insensitivity to the L\u2010type Ca<jats:sup>2+<\/jats:sup>channel blocker nifedipine (1 \u03bc<jats:sc>m<\/jats:sc>) (100 \u00b1 29%). Spontaneous depolarizations were abolished by the P2X<jats:sub>1<\/jats:sub>receptor antagonist NF449 (10 \u03bc<jats:sc>m<\/jats:sc>) (frequency 8.5 \u00b1 8.5% of controls), insensitive to the muscarinic acetylcholine receptor antagonist atropine (1 \u03bc<jats:sc>m<\/jats:sc>) (103.4 \u00b1 3.0%), and became more frequent in latrotoxin (LTX; 1 n<jats:sc>m<\/jats:sc>) (438 \u00b1 95%), suggesting that they are spontaneous excitatory junction potentials (sEJPs). Such sEJPs were correlated, in amplitude and timing, with focal Ca<jats:sup>2+<\/jats:sup>transients in smooth muscle cells (measured using confocal microscopy), suggesting a common origin: ATP binding to P2X<jats:sub>1<\/jats:sub>receptors. sAPs were abolished by NF449, insensitive to atropine (126 \u00b1 39%) and increased in frequency by LTX (930 \u00b1 450%) suggesting a neurogenic, purinergic origin, in common with sEJPs. By comparing the kinetics of sAPs and sEJPs, we demonstrated that sAPs occur when sufficient cation influx through P2X<jats:sub>1<\/jats:sub>receptors triggers L\u2010type Ca<jats:sup>2+<\/jats:sup>channels; the first peak of the differentiated rising phase of depolarizations \u2013 attributed to the influx of cations through the P2X<jats:sub>1<\/jats:sub>receptor \u2013 is of larger amplitude for sAPs (2248 mV s<jats:sup>\u22121<\/jats:sup>) than sEJPs (439 mV s<jats:sup>\u22121<\/jats:sup>). Surprisingly, sAPs in the mouse urinary bladder, unlike those from other species, are triggered by stochastic ATP release from parasympathetic nerve terminals rather than being myogenic.<\/jats:p>","DOI":"10.1113\/jphysiol.2008.162040","type":"journal-article","created":{"date-parts":[[2008,10,21]],"date-time":"2008-10-21T00:24:34Z","timestamp":1224548674000},"page":"5743-5755","source":"Crossref","is-referenced-by-count":43,"title":["Spontaneous purinergic neurotransmission in the mouse urinary bladder"],"prefix":"10.1113","volume":"586","author":[{"given":"John S.","family":"Young","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"En","family":"Meng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tom C.","family":"Cunnane","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keith 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