{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T23:24:05Z","timestamp":1771629845926,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[1994,5,1]]},"abstract":"<jats:p> 1. Transmembrane ion movements upon sodium-pump inhibition were studied in identified neurons of the subesophageal ganglia of Helix aspersa. A two-microelectrode, voltage-clamp technique was used to measure transmembrane currents. Changes in intracellular Na+, K+, and Ca2+ concentrations were measured, in unclamped neurons, with Na(+)-sensitive microelectrodes, K(+)-sensitive microelectrodes, and with the fluorescent probe fura-2, respectively. 2. Inhibition of the sodium pump with ouabain (1 mM) elicited an increase in intracellular Na+ concentration, [Na+]i, at an initial rate of 0.42 +\/- 0.05 mM\/min (mean +\/- SE; n = 27), and a membrane depolarization often followed by hyperpolarization. In cells clamped at -50 or -60 mV, ouabain produced an inward shift in membrane-holding current followed by an outward current usually having two components, transient and sustained, respectively. 3. Replacing external Na+ with either N-methyl-D-glucammonium or tetraethylammonium (TEA+) abolished both the ouabain-induced inward membrane current and the rise in [Na+]i, suggesting that Na+ was the charge carrier of the inward current. 4. Cd2+ (400 microM) reduced the rate of rise of the inward current by 60% and the estimated net Na+ flux by 47%. 5. The outward current was abolished by K(+)-channel blockers (10 mM TEA+ and 5 mM 4-aminopyridine or 10 nM apamin). Cd2+ (400 microM), a Ca(2+)-entry blocker, also abolished the outward current. 6. Inhibition of the sodium pump elicited a fall in [K+]i at an initial rate of 1.4 +\/- 0.2 mM\/min (n = 9 cells). 7. Upon inhibition of the sodium pump in neurons loaded with fura-2, [Ca2+]i increased from an estimated resting level of 147 +\/- 37 nM to a maximum of 764 +\/- 248 nM (n = 12 cells). 8. The rise in [Ca2+]i in the sustained presence of ouabain was transient, lasting 19.5 +\/- 2.8 min, and could be prevented by removal of external Ca2+ before ouabain application or curtailed by removal of external Ca2+ during sustained ouabain exposure. The latter effect was not a consequence of exhaustion of caffeine-sensitive intracellular Ca2+ stores. 9. It is concluded that 1) the rise in [Ca2+]i upon Na(+)-pump inhibition requires the presence of external Ca2+, 2) the outward current observed upon pump inhibition is a Ca(2+)-activated K+ current flowing through apamin-sensitive channels, 3) the resting Na+ permeability involves a Cd(2+)-sensitive component, 4) a large fraction (approximately 30\u201360%) of the previously described ouabain-induced cell shrinkage may result from Ca(2+)-activated K+ efflux contributing to net solute and water loss. <\/jats:p>","DOI":"10.1152\/jn.1994.71.5.1787","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T22:35:01Z","timestamp":1514154901000},"page":"1787-1796","source":"Crossref","is-referenced-by-count":19,"title":["Transmembrane ion movements elicited by sodium pump inhibition in Helix aspersa neurons"],"prefix":"10.1152","volume":"71","author":[{"given":"F. J.","family":"Alvarez-Leefmans","sequence":"first","affiliation":[{"name":"Departamento de Neurobiologia, Instituto Mexicano de Psiquiatria, Mexico, D.F."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H.","family":"Cruzblanca","sequence":"additional","affiliation":[{"name":"Departamento de Neurobiologia, Instituto Mexicano de Psiquiatria, Mexico, D.F."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S. M.","family":"Gamino","sequence":"additional","affiliation":[{"name":"Departamento de Neurobiologia, Instituto Mexicano de Psiquiatria, Mexico, D.F."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Altamirano","sequence":"additional","affiliation":[{"name":"Departamento de Neurobiologia, Instituto Mexicano de Psiquiatria, Mexico, D.F."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Nani","sequence":"additional","affiliation":[{"name":"Departamento de Neurobiologia, Instituto Mexicano de Psiquiatria, Mexico, D.F."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L.","family":"Reuss","sequence":"additional","affiliation":[{"name":"Departamento de Neurobiologia, Instituto Mexicano de Psiquiatria, Mexico, D.F."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","container-title":["Journal of Neurophysiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/jn.1994.71.5.1787","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T01:18:59Z","timestamp":1567991939000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/jn.1994.71.5.1787"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1994,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1994,5,1]]}},"alternative-id":["10.1152\/jn.1994.71.5.1787"],"URL":"https:\/\/doi.org\/10.1152\/jn.1994.71.5.1787","relation":{},"ISSN":["0022-3077","1522-1598"],"issn-type":[{"value":"0022-3077","type":"print"},{"value":"1522-1598","type":"electronic"}],"subject":[],"published":{"date-parts":[[1994,5,1]]}}}