{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T07:54:28Z","timestamp":1791100468556,"version":"4.1.0"},"reference-count":78,"publisher":"Society for Neuroscience","issue":"42","license":[{"start":{"date-parts":[[2012,4,19]],"date-time":"2012-04-19T00:00:00Z","timestamp":1334793600000},"content-version":"vor","delay-in-days":183,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2011,10,19]]},"abstract":"<jats:p>We explored whether nicotinic acetylcholine receptors (nAChRs) might participate in paracrine transmission by asking if they respond to spillover of ACh at a model synapse in the chick ciliary ganglion, where ACh activates diffusely distributed \u03b17- and \u03b13-containing nAChRs (\u03b17-nAChRs and \u03b13*-nAChRs). Elevating quantal content lengthened EPSC decay time and prolonged both the fast (\u03b17-nAChR-mediated) and slow (\u03b13*-nAChR-mediated) components of decay, even in the presence of acetylcholinesterase. Increasing quantal content also prolonged decay times of pharmacologically isolated \u03b17-nAChR- and \u03b13*-nAChR-EPSCs. The effect upon EPSC decay time of changing quantal content was 5\u201310 times more pronounced for \u03b13*-nAChR- than \u03b17-nAChR-mediated currents and operated over a considerably longer time window: \u223c20 vs \u223c2 ms. Control experiments rule out a presynaptic source for the effect. We suggest that \u03b13*-nAChR currents are prolonged at higher quantal content because of ACh spillover and postsynaptic potentiation (Hartzell et al., 1975), while \u03b17-nAChR currents are prolonged probably for other reasons, e.g., increased occupancy of long channel open states. \u03b13*-nAChRs report more spillover when \u03b17-nAChRs are competitively blocked than under native conditions; this could be explained if \u03b17-nAChRs buffer ACh and regulate its availability to activate \u03b13*-nAChRs. Our results suggest that non-\u03b17-nAChRs such as \u03b13*-nAChRs may be suitable for paracrine nicotinic signaling but that \u03b17-nAChRs may not be suitable. Our results further suggest that \u03b17-nAChRs may buffer ACh and regulate its bioavailability.<\/jats:p>","DOI":"10.1523\/jneurosci.3400-11.2011","type":"journal-article","created":{"date-parts":[[2011,10,19]],"date-time":"2011-10-19T21:18:14Z","timestamp":1319059094000},"page":"14920-14930","source":"Crossref","is-referenced-by-count":14,"title":["\u03b17-Containing and Non-\u03b17-Containing Nicotinic Receptors Respond Differently to Spillover of Acetylcholine"],"prefix":"10.1523","volume":"31","author":[{"given":"Doychin","family":"Stanchev","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter 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