{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T21:11:32Z","timestamp":1778274692307,"version":"3.51.4"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[1996,6,1]]},"abstract":"<jats:p> 1. The role of voltage-gated calcium channels in the generation of activity-induced alkaline shifts in extracellular pH (pHo) was studied in rat hippocampal slices (area CAI) by means of Ca(2+)-and H(+)-selective microlectrodes inserted into the stratum pyramidale and\/or stratum radiatum. 2. After complete pharmacological blockade of ionotropic glutamate receptors and gamma-aminobutyric acid-A (GABAA) receptors, trains (5-10 Hz, 5-10s) of antidromic spikes in pyramidal neurons were associated with a fast alkaline transient of up to 0.17 pH units and a fall in the extracellular Ca2+ concentration ([Ca2+]o). The alkaline shift was strongly enhanced upon inhibition of extracellular carbonic anhydrase. 3. Application of 100 microM Ni2+ plus 100 microM Cd2+ inhibited both the fall in [Ca2+]o and the alkaline transient triggered by antidromic spikes. The alkaline shift was abolished in the absence of extracellular Ca2+. 4. In the absence of postsynaptic receptor antagonists, alkaline transients linked to a given level of synaptic excitation in s. radiatum were strongly suppressed after blockade of somatic (and, consequently, of dendritic \u201cbackpropagating\u201d) spikes by microdrop application of tetrodotoxin to the cell-body layer. 5. We have previously shown that activity-induced alkaline transients in the CAI region are due to an influx of Ca2+ into neurons, which triggers an influx of H+ ions probably caused by activation of a plasmalemmal Ca2+\/H+ ATPase. The present results indicate that much (in s. pyramidale perhaps all) of the pH-changing influx of Ca2+ is mediated by voltage-gated Ca2+ channels. <\/jats:p>","DOI":"10.1152\/jn.1996.75.6.2354","type":"journal-article","created":{"date-parts":[[2017,12,25]],"date-time":"2017-12-25T00:45:28Z","timestamp":1514162728000},"page":"2354-2360","source":"Crossref","is-referenced-by-count":25,"title":["Role of voltage-gated calcium channels in the generation of activity-induced extracellular pH transients in the rat hippocampal slice"],"prefix":"10.1152","volume":"75","author":[{"given":"P.","family":"Paalasmaa","sequence":"first","affiliation":[{"name":"Department of Biosciences, University of Helsinki, Finland."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Kaila","sequence":"additional","affiliation":[{"name":"Department of Biosciences, University of Helsinki, Finland."}],"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.1996.75.6.2354","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T05:27:00Z","timestamp":1568006820000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/jn.1996.75.6.2354"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1996,6,1]]}},"alternative-id":["10.1152\/jn.1996.75.6.2354"],"URL":"https:\/\/doi.org\/10.1152\/jn.1996.75.6.2354","relation":{},"ISSN":["0022-3077","1522-1598"],"issn-type":[{"value":"0022-3077","type":"print"},{"value":"1522-1598","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,6,1]]}}}