{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,30]],"date-time":"2025-11-30T13:48:38Z","timestamp":1764510518526},"reference-count":44,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2015,10]]},"abstract":" In this study, we examined the functional coupling between Na+<\/jats:sup>-activated potassium (KNa<\/jats:sub>) channels and Na+<\/jats:sup> influx through voltage-dependent Na+<\/jats:sup> channels in Kenyon cells isolated from the mushroom body of the cricket Gryllus bimaculatus. Single-channel activity of KNa<\/jats:sub> channels was recorded with the cell-attached patch configuration. The open probability ( Po<\/jats:sub>) of KNa<\/jats:sub> channels increased with increasing Na+<\/jats:sup> concentration in a bath solution, whereas it decreased by the substitution of Na+<\/jats:sup> with an equimolar concentration of Li+<\/jats:sup>. The Po<\/jats:sub> of KNa<\/jats:sub> channels was also found to be reduced by bath application of a high concentration of TTX (1 \u03bcM) and riluzole (100 \u03bcM), which inhibits both fast ( INaf<\/jats:sub>) and persistent ( INaP<\/jats:sub>) Na+<\/jats:sup> currents, whereas it was unaffected by a low concentration of TTX (10 nM), which selectively blocks INaf<\/jats:sub>. Bath application of Cd2+<\/jats:sup> at a low concentration (50 \u03bcM), as an inhibitor of INaP<\/jats:sub>, also decreased the Po<\/jats:sub> of KNa<\/jats:sub> channels. Conversely, bath application of the inorganic Ca2+<\/jats:sup>-channel blockers Co2+<\/jats:sup> and Ni2+<\/jats:sup> at high concentrations (500 \u03bcM) had little effect on the Po<\/jats:sub> of KNa<\/jats:sub> channels, although Cd2+<\/jats:sup> (500 \u03bcM) reduced the Po<\/jats:sub> of KNa<\/jats:sub> channels. Perforated whole cell clamp analysis further indicated the presence of sustained outward currents for which amplitude was dependent on the amount of Na+<\/jats:sup> influx. Taken together, these results indicate that KNa<\/jats:sub> channels could be activated by Na+<\/jats:sup> influx passing through voltage-dependent persistent Na+<\/jats:sup> channels. The functional significance of this coupling mechanism was discussed in relation to the membrane excitability of Kenyon cells and its possible role in the formation of long-term memory. <\/jats:p>","DOI":"10.1152\/jn.00087.2015","type":"journal-article","created":{"date-parts":[[2015,8,12]],"date-time":"2015-08-12T22:39:54Z","timestamp":1439419194000},"page":"2450-2459","source":"Crossref","is-referenced-by-count":12,"title":["Functional coupling between sodium-activated potassium channels and voltage-dependent persistent sodium currents in cricket Kenyon cells"],"prefix":"10.1152","volume":"114","author":[{"given":"Izumi","family":"Takahashi","sequence":"first","affiliation":[{"name":"Department of Biology, Tokyo Gakugei University, Tokyo, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masami","family":"Yoshino","sequence":"additional","affiliation":[{"name":"Department of Biology, Tokyo Gakugei University, Tokyo, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/jn.90459.2008"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(03)00639-1"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/317540a0"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.23-37-11681.2003"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2010.00133"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1998.743bj.x"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-5793(02)03653-0"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/nn.2313"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1997.001bf.x"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.5978-08.2009"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1993.sp019559"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1991.sp018522"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1016\/0166-2236(94)90093-0"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1989.sp017533"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.12-05-01964.1992"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(94)91024-3"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.5088-11.2012"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1007\/BF00376215"},{"key":"B19","unstructured":"Hille B. 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