{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T15:49:55Z","timestamp":1761580195551},"reference-count":44,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2004,5]]},"abstract":"<jats:p>Electrophysiological and microfluorimetric techniques were used to determine whether intracellular photorelease of caged IP<jats:sub>3<\/jats:sub>, and the consequent release of Ca<jats:sup>2+<\/jats:sup>, could trigger a Ca<jats:sup>2+<\/jats:sup>-activated K<jats:sup>+<\/jats:sup>current ( I<jats:sub>IP3<\/jats:sub>). Photorelease of caged IP<jats:sub>3<\/jats:sub>evoked an I<jats:sub>IP3<\/jats:sub>that averaged 2.36 \u00b1 0.35 (SE) pA\/pF in 24 of 28 rabbit primary vagal sensory neurons (nodose ganglion neurons, NGNs) voltage-clamped at \u201350 mV. I<jats:sub>IP3<\/jats:sub>was abolished by intracellular BAPTA (2 mM), a Ca<jats:sup>2+<\/jats:sup>chelator. Changing the K<jats:sup>+<\/jats:sup>equilibrium potential by increasing extracellular K<jats:sup>+<\/jats:sup>ion concentration caused a predicted Nernstian shift in the reversal potential of I<jats:sub>IP3<\/jats:sub>. These results indicated that I<jats:sub>IP3<\/jats:sub>was a Ca<jats:sup>2+<\/jats:sup>-dependent K<jats:sup>+<\/jats:sup>current. I<jats:sub>IP3<\/jats:sub>was unaffected by three common antagonists of Ca<jats:sup>2+<\/jats:sup>-activated K<jats:sup>+<\/jats:sup>currents: bath-applied iberiotoxin (50 nM) or apamin (100 nM), and intracellular 8-Br-cAMP (100 \u03bcM) included in the patch pipette. We have previously demonstrated that both IP<jats:sub>3<\/jats:sub>-evoked Ca<jats:sup>2+<\/jats:sup>release and Ca<jats:sup>2+<\/jats:sup>-induced Ca<jats:sup>2+<\/jats:sup>release (CICR) are co-expressed in NGNs and that CICR can trigger a Ca<jats:sup>2+<\/jats:sup>-activated K<jats:sup>+<\/jats:sup>current. In the present study, using caffeine, a CICR agonist, to selectively attenuate intracellular Ca<jats:sup>2+<\/jats:sup>stores, we showed that IP<jats:sub>3<\/jats:sub>-evoked Ca<jats:sup>2+<\/jats:sup>release occurs independently of CICR, but interestingly, that a component of I<jats:sub>IP3<\/jats:sub>requires CICR. These data suggest that IP<jats:sub>3<\/jats:sub>-evoked Ca<jats:sup>2+<\/jats:sup>release activates a K<jats:sup>+<\/jats:sup>current that is pharmacologically distinct from other Ca<jats:sup>2+<\/jats:sup>-activated K<jats:sup>+<\/jats:sup>currents in NGNs. We describe several models that explain our results based on Ca<jats:sup>2+<\/jats:sup>signaling microdomains in NGNs.<\/jats:p>","DOI":"10.1152\/jn.01008.2003","type":"journal-article","created":{"date-parts":[[2004,4,7]],"date-time":"2004-04-07T02:13:14Z","timestamp":1081303994000},"page":"2344-2352","source":"Crossref","is-referenced-by-count":14,"title":["Localized IP<sub>3<\/sub>-Evoked Ca<sup>2+<\/sup>Release Activates a K<sup>+<\/sup>Current in Primary Vagal Sensory Neurons"],"prefix":"10.1152","volume":"91","author":[{"given":"Robert E.","family":"Hoesch","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel","family":"Weinreich","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joseph P. 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