{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T17:31:27Z","timestamp":1790271087228,"version":"4.1.0"},"reference-count":53,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[1997,12,1]]},"abstract":"<jats:p>Rose, Christine R., Bruce R. Ransom, and Stephan G. Waxman. Pharmacological characterization of Na<jats:sup>+<\/jats:sup>influx via voltage-gated Na<jats:sup>+<\/jats:sup>channels in spinal cord astrocytes. J. Neurophysiol. 78: 3249\u20133258, 1997. Spinal cord astrocytes display a high density of voltage-gated Na<jats:sup>+<\/jats:sup>channels. To study the contribution of Na<jats:sup>+<\/jats:sup>influx via these channels to Na<jats:sup>+<\/jats:sup>homeostasis in cultured spinal cord astrocytes, we measured intracellular Na<jats:sup>+<\/jats:sup>concentration ([Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>) with the fluorescent dye sodium-binding benzofuran isophthalate. Stellate and nonstellate astrocytes, which display Na<jats:sup>+<\/jats:sup>currents with different properties, were differentiated. Baseline [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>was 8.5 mM in these cells and was not altered by 100 \u03bcM tetrodotoxin (TTX). Inhibition of Na<jats:sup>+<\/jats:sup>channel inactivation by veratridine (100 \u03bcM) evoked a [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>increase of 47.1 mM in 44% of stellate and 9.7 mM in 64% of nonstellate astrocytes. About 30% of cells reacted to veratridine with a [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>decrease of \u223c2 mM. Qualitatively similar [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>changes were caused by aconitine. The effects of veratridine were blocked by TTX, amplified by (\u03b1-)scorpion toxin and usually were readily reversible. Veratridine-induced [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>increases were reduced upon membrane depolarization with elevated extracellular [K<jats:sup>+<\/jats:sup>]. Recovery to baseline [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>was unaltered during blocking of K<jats:sup>+<\/jats:sup>channels with 4-aminopyridine. [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>increases evoked by the ionotropic non- N-methyl-d-aspartate receptor agonist kainate were not altered by TTX. Our results indicate that influx of Na<jats:sup>+<\/jats:sup>via voltage- gated Na<jats:sup>+<\/jats:sup>channels is not a prerequisite for glial Na<jats:sup>+<\/jats:sup>,K<jats:sup>+<\/jats:sup>-ATPase activity in spinal cord astrocytes at rest nor does it seem to be involved in [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>increases evoked by kainate. During pharmacological inhibition of Na<jats:sup>+<\/jats:sup>channel inactivation, however, Na<jats:sup>+<\/jats:sup>channels can serve as prominent pathways of Na<jats:sup>+<\/jats:sup>influx and mediate large perturbations in [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>, suggesting that Na<jats:sup>+<\/jats:sup>channel inactivation plays an important functional role in these cells.<\/jats:p>","DOI":"10.1152\/jn.1997.78.6.3249","type":"journal-article","created":{"date-parts":[[2017,12,25]],"date-time":"2017-12-25T07:19:17Z","timestamp":1514186357000},"page":"3249-3258","source":"Crossref","is-referenced-by-count":17,"title":["Pharmacological Characterization of Na<sup>+<\/sup>Influx via Voltage-Gated Na<sup>+<\/sup>Channels in Spinal Cord Astrocytes"],"prefix":"10.1152","volume":"78","author":[{"given":"Christine R.","family":"Rose","sequence":"first","affiliation":[{"name":"Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06520;"},{"name":"Neuroscience Research Center, Veterans Affairs Hospital, West Haven, Connecticut 06516; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce R.","family":"Ransom","sequence":"additional","affiliation":[{"name":"Department of Neurology, University of Washington School of Medicine, Seattle, Washington 98195-6465"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen G.","family":"Waxman","sequence":"additional","affiliation":[{"name":"Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06520;"},{"name":"Neuroscience Research Center, Veterans Affairs Hospital, West Haven, Connecticut 06516; and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0896-6273(93)90145-H"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1002\/jnr.490220307"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1987.sp016361"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0896-6273(89)90076-7"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ne.13.030190.002301"},{"key":"B6","first-page":"S3","volume":"41","author":"Berwald-Netter Y.","year":"1983","journal-title":"J. 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